- Published on
Pathology - Uterine leiomyomas
Definition
Synonym • Fibroids. • Benign neoplasms of smooth muscle originating in the myometrium.
Epidemiology • Highly prevalent tumors identified in up to 75% of all women. Approximately 20% of women are affected by symptomatic fibroids. Aetiology The exact etiology remains ambiguous; nevertheless, contributing factors encompass race and parity, with black and nulliparous women exhibiting a higher susceptibility.
Pathogenesis • Hormonal tumors that predominantly affect women of reproductive age, exhibit rapid growth during pregnancy, and undergo regression post-menopause. Genetic research indicates that they are clonal neoplasms characterized by chromosomal abnormalities.
Presentation: Menorrhagia. • Subfertility: this is likely attributable to endometrial deformation, hindering implantation. • Pelvic pain: this may be associated with tumor infarction or torsion of a pedunculated fibroid. • Palpable mass: fibroids may attain sufficient size to be discerned abdominally.
Macroscopy • Well-defined, white, whorled tumors that typically protrude from the adjacent myometrium upon incision. • Frequently numerous and may be intramural or extend from the serosal surface (subserosal) or into the uterine cavity (submucosal). • Calcification is prevalent. Infarcted tumors exhibit a red coloration instead of white, a phenomenon referred to as 'red degeneration.'
Histopathology Classical fibroids consist of interlacing fascicles of unremarkable smooth muscle cells characterized by blunt-ended nuclei and eosinophilic cytoplasm. Regions of hyalinization and calcification are prevalent. Numerous histological variants are well-documented, all exhibiting benign behavior. These encompass cellular leiomyoma, highly cellular leiomyoma, mitotically active leiomyoma, and atypical leiomyoma.
Prognosis: Benign tumors exhibit no potential for malignant behavior. Uterine leiomyosarcoma Uterine leiomyosarcoma is a malignant neoplasm of smooth muscle originating in the myometrium. While rare, it constitutes the most prevalent uterine sarcoma. The swift growth of a uterine tumor may raise concerns for leiomyosarcoma; nevertheless, many cases are not identified prior to surgery and are presumed to be big fibroids.
Macroscopically, leiomyosarcomas are inadequately defined and typically do not protrude from the adjacent myometrium due to their infiltrative characteristics. They are more pliable than fibroids and may exhibit signs of necrosis.
Histologically, leiomyosarcomas are neoplasms of smooth muscle that exhibit several abnormal characteristics, including widespread cytological atypia, necrosis of tumor cells, and elevated mitotic activity. Leiomyosarcomas are aggressive tumors characterized by a propensity for local recurrence and metastasis, especially to the liver and lungs.
Definition
Synonym • Fibroids. • Benign neoplasms of smooth muscle originating in the myometrium.
Epidemiology • Highly prevalent tumors identified in up to 75% of all women. Approximately 20% of women are affected by symptomatic fibroids. Aetiology The exact etiology remains ambiguous; nevertheless, contributing factors encompass race and parity, with black and nulliparous women exhibiting a higher susceptibility.
Pathogenesis • Hormonal tumors that predominantly affect women of reproductive age, exhibit rapid growth during pregnancy, and undergo regression post-menopause. Genetic research indicates that they are clonal neoplasms characterized by chromosomal abnormalities.
Presentation: Menorrhagia. • Subfertility: this is likely attributable to endometrial deformation, hindering implantation. • Pelvic pain: this may be associated with tumor infarction or torsion of a pedunculated fibroid. • Palpable mass: fibroids may attain sufficient size to be discerned abdominally.
Macroscopy • Well-defined, white, whorled tumors that typically protrude from the adjacent myometrium upon incision. • Frequently numerous and may be intramural or extend from the serosal surface (subserosal) or into the uterine cavity (submucosal). • Calcification is prevalent. Infarcted tumors exhibit a red coloration instead of white, a phenomenon referred to as 'red degeneration.'
Histopathology Classical fibroids consist of interlacing fascicles of unremarkable smooth muscle cells characterized by blunt-ended nuclei and eosinophilic cytoplasm. Regions of hyalinization and calcification are prevalent. Numerous histological variants are well-documented, all exhibiting benign behavior. These encompass cellular leiomyoma, highly cellular leiomyoma, mitotically active leiomyoma, and atypical leiomyoma.
Prognosis: Benign tumors exhibit no potential for malignant behavior. Uterine leiomyosarcoma Uterine leiomyosarcoma is a malignant neoplasm of smooth muscle originating in the myometrium. While rare, it constitutes the most prevalent uterine sarcoma. The swift growth of a uterine tumor may raise concerns for leiomyosarcoma; nevertheless, many cases are not identified prior to surgery and are presumed to be big fibroids.
Macroscopically, leiomyosarcomas are inadequately defined and typically do not protrude from the adjacent myometrium due to their infiltrative characteristics. They are more pliable than fibroids and may exhibit signs of necrosis.
Histologically, leiomyosarcomas are neoplasms of smooth muscle that exhibit several abnormal characteristics, including widespread cytological atypia, necrosis of tumor cells, and elevated mitotic activity. Leiomyosarcomas are aggressive tumors characterized by a propensity for local recurrence and metastasis, especially to the liver and lungs.
- Published on
Pathology - Functional ovarian cysts
Definition • Ovarian follicles exhibiting pathogenic cystic alterations. • A suggested threshold distinguishing normal cystic follicles from functional cysts is 2.5 cm.
Terminology: Cysts originating from pre-ovulatory follicles are termed follicular cysts, whereas those arising from the corpus luteum are referred to as corpus luteum cysts.
Epidemiology: Highly prevalent.
Aetiology • Follicular cysts are believed to indicate dysfunction of the pituitary-ovarian axis. Corpus luteum cysts arise from severe hemorrhage within a corpus luteum.
Presentation • Nearly all are identified incidentally, either through imaging or by a surgeon examining the pelvis. • Large cysts may intermittently manifest as a pelvic mass. Macroscopy: Follicular cysts are often solitary and range in size from 2.5 to 10 cm. The structures are characterized by smooth contours and contain a transparent fluid. Corpus luteum cysts typically range in size from 2.5 to 5 cm. The cyst contains sanguineous fluid, and the wall is frequently yellow
Cytopathology . : The aspirated fluid from a follicular cyst comprises many granulosa cells characterized by spherical nuclei, coarse chromatin, and a narrow rim of cytoplasm. Nuclear grooves may be observed. Certain cysts may also comprise luteinized cells. Aspirated fluid from a corpus luteum cyst comprises blood, haemosiderin-laden macrophages, and many completely luteinized granulosa cells. These are sizable polyhedral cells characterized by copious finely granular cytoplasm. The nuclei are round to elliptical, exhibiting finely granular chromatin and conspicuous nucleoli. Nuclear grooves are absent. Histopathology Follicular cysts are composed of granulosa and theca cells, which may exhibit luteinization. Corpus luteum cysts have significant central hemorrhage. The lining consists of entirely luteinized granulosa and theca cells.
Prognosis: Functional ovarian cysts are completely benign. They are mostly of clinical significance, as big cysts may raise suspicion for a cystic neoplasm.
Definition • Ovarian follicles exhibiting pathogenic cystic alterations. • A suggested threshold distinguishing normal cystic follicles from functional cysts is 2.5 cm.
Terminology: Cysts originating from pre-ovulatory follicles are termed follicular cysts, whereas those arising from the corpus luteum are referred to as corpus luteum cysts.
Epidemiology: Highly prevalent.
Aetiology • Follicular cysts are believed to indicate dysfunction of the pituitary-ovarian axis. Corpus luteum cysts arise from severe hemorrhage within a corpus luteum.
Presentation • Nearly all are identified incidentally, either through imaging or by a surgeon examining the pelvis. • Large cysts may intermittently manifest as a pelvic mass. Macroscopy: Follicular cysts are often solitary and range in size from 2.5 to 10 cm. The structures are characterized by smooth contours and contain a transparent fluid. Corpus luteum cysts typically range in size from 2.5 to 5 cm. The cyst contains sanguineous fluid, and the wall is frequently yellow
Cytopathology . : The aspirated fluid from a follicular cyst comprises many granulosa cells characterized by spherical nuclei, coarse chromatin, and a narrow rim of cytoplasm. Nuclear grooves may be observed. Certain cysts may also comprise luteinized cells. Aspirated fluid from a corpus luteum cyst comprises blood, haemosiderin-laden macrophages, and many completely luteinized granulosa cells. These are sizable polyhedral cells characterized by copious finely granular cytoplasm. The nuclei are round to elliptical, exhibiting finely granular chromatin and conspicuous nucleoli. Nuclear grooves are absent. Histopathology Follicular cysts are composed of granulosa and theca cells, which may exhibit luteinization. Corpus luteum cysts have significant central hemorrhage. The lining consists of entirely luteinized granulosa and theca cells.
Prognosis: Functional ovarian cysts are completely benign. They are mostly of clinical significance, as big cysts may raise suspicion for a cystic neoplasm.
- Published on
Pathology - Polycystic Ovary Syndrome
Definition: A metabolic syndrome characterized by testosterone excess, ovulatory dysfunction, and, in certain women, the presence of polycystic ovaries.
Epidemiology • Prevalent, impacting approximately 5% of women. Aetiology Insulin resistance seems to be the principal underlying reason
Pathogenesis • Insulin resistance, obesity, and increased androgen synthesis by the ovaries. • Androgens contribute to hirsutism, acne, and irregular follicle maturation. • Irregular follicle maturation may result in polycystic ovaries in certain women. • Chronic anovulation leads to subfertility and decreased estrogen production. • Prolonged estrogen exposure results in endometrial hyperplasia and increases the chance of developing endometrial intraepithelial neoplasia and endometrial carcinoma
Presentation • Subfertility is a prevalent manifestation. • Certain women exhibit hirsutism and acne.
Radiology • Polycystic ovaries may be observed in certain women, but not universally. Biochemistry • Increased blood androgen levels. • Diminished glucose tolerance or overt diabetes.
Prognosis • The primary concerns are the difficulties linked to obesity and the possibility of endometrial carcinoma. • Weight loss, insulin-sensitizing medications, and progesterone therapy all contribute to mitigating these complications.
Definition: A metabolic syndrome characterized by testosterone excess, ovulatory dysfunction, and, in certain women, the presence of polycystic ovaries.
Epidemiology • Prevalent, impacting approximately 5% of women. Aetiology Insulin resistance seems to be the principal underlying reason
Pathogenesis • Insulin resistance, obesity, and increased androgen synthesis by the ovaries. • Androgens contribute to hirsutism, acne, and irregular follicle maturation. • Irregular follicle maturation may result in polycystic ovaries in certain women. • Chronic anovulation leads to subfertility and decreased estrogen production. • Prolonged estrogen exposure results in endometrial hyperplasia and increases the chance of developing endometrial intraepithelial neoplasia and endometrial carcinoma
Presentation • Subfertility is a prevalent manifestation. • Certain women exhibit hirsutism and acne.
Radiology • Polycystic ovaries may be observed in certain women, but not universally. Biochemistry • Increased blood androgen levels. • Diminished glucose tolerance or overt diabetes.
Prognosis • The primary concerns are the difficulties linked to obesity and the possibility of endometrial carcinoma. • Weight loss, insulin-sensitizing medications, and progesterone therapy all contribute to mitigating these complications.
- Published on
Pathology - Ovarian benign tumors
Cystic teratoma in maturity Benign germ cell ovarian tumors, sometimes referred to as "dermoid cysts," are most common in young women aged 20 to 29. • Larger tumors may cause pelvic pain, but many are asymptomatic and found by accident. Torsion or rupture, which results in an acute abdomen, is the most dangerous consequence. • The tumor appears cystic from a macroscopic perspective and contains a soft, greasy yellow substance. Teeth, bone, cartilage, and hair may be apparent. • According to histology, the tumor is made up of mature adult-type tissues of almost any kind, such as cartilage, smooth muscle, fat, skin, brain, respiratory, and gastrointestinal tissue.Although they are far less common, the majority of other germ cell ovarian tumors (such as dysgerminoma and immature teratoma) exhibit malignant behavior.
Cystadenoma serous -Benign epithelial ovarian tumors typically affect premenopausal women. They can be discovered by chance when a pelvic mass or an acute abdomen from torsion is present. They can be unilocular or multilocular in appearance. Histologically, the cysts are lined by a single layer of bland columnar cells, which may be ciliated or non-ciliated. The cysts contain clear fluid and have a thin wall with a smooth lining.
Cystomatous mucinous tumor • Premenopausal women typically develop benign epithelial ovarian tumors. • It may be discovered by chance when there are signs of a pelvic mass or an acute abdomen brought on by torsion. • On a macroscopic level, the tumor is often unilateral and measures 10 cm on average, though there have been cases of enormous tumors. One or more cysts filled with viscous mucoid material make up the tumor. • A single layer of bland columnar cells, either intestinal or endocervical in origin, lines the cysts histologically.
Ovarian Fibroma
Benign sex-cord stromal ovarian tumors, which are made of collagen and fibrocytes, can occur in a variety of age groups, although the majority are found in women over 50. They are frequently found by accident and are little. Ascites and stomach pain may result from a large tumor. • From a macroscopic perspective, the tumor has a solid white sliced surface. • According to histology, the tumor is made up of bland spindled cells that are expanding within a collagenous stroma.
Ovarian tumors that are borderline epithelial
A class of epithelial tumors known as borderline epithelial ovarian tumors tends to behave indolently yet shows more marked proliferation than benign epithelial tumors. Serous (borderline serous) tumors make up the great bulk of borderline epithelial tumors. At the macroscopic level, they are enormous, often bilateral, cystic tumors that are typically multifocal. Numerous papillary excrescences protrude from the cysts' surface. The tumors exhibit low-grade nuclear atypia and are histologically formed of complicated branching papillae covered by proliferating columnar epithelial cells. The existence of tiny tumor "implants" in the peritoneum or omentum in around 15% to 30% of cases is an odd characteristic of borderline serous tumors. These implants can be classified as either invasive or non-invasive histologically. The majority are non-invasive, and the prognosis for these patients is typically favorable. Although invasive implants are extremely uncommon, they are typically linked to a poor prognosis
Cystic teratoma in maturity Benign germ cell ovarian tumors, sometimes referred to as "dermoid cysts," are most common in young women aged 20 to 29. • Larger tumors may cause pelvic pain, but many are asymptomatic and found by accident. Torsion or rupture, which results in an acute abdomen, is the most dangerous consequence. • The tumor appears cystic from a macroscopic perspective and contains a soft, greasy yellow substance. Teeth, bone, cartilage, and hair may be apparent. • According to histology, the tumor is made up of mature adult-type tissues of almost any kind, such as cartilage, smooth muscle, fat, skin, brain, respiratory, and gastrointestinal tissue.Although they are far less common, the majority of other germ cell ovarian tumors (such as dysgerminoma and immature teratoma) exhibit malignant behavior.
Cystadenoma serous -Benign epithelial ovarian tumors typically affect premenopausal women. They can be discovered by chance when a pelvic mass or an acute abdomen from torsion is present. They can be unilocular or multilocular in appearance. Histologically, the cysts are lined by a single layer of bland columnar cells, which may be ciliated or non-ciliated. The cysts contain clear fluid and have a thin wall with a smooth lining.
Cystomatous mucinous tumor • Premenopausal women typically develop benign epithelial ovarian tumors. • It may be discovered by chance when there are signs of a pelvic mass or an acute abdomen brought on by torsion. • On a macroscopic level, the tumor is often unilateral and measures 10 cm on average, though there have been cases of enormous tumors. One or more cysts filled with viscous mucoid material make up the tumor. • A single layer of bland columnar cells, either intestinal or endocervical in origin, lines the cysts histologically.
Ovarian Fibroma
Benign sex-cord stromal ovarian tumors, which are made of collagen and fibrocytes, can occur in a variety of age groups, although the majority are found in women over 50. They are frequently found by accident and are little. Ascites and stomach pain may result from a large tumor. • From a macroscopic perspective, the tumor has a solid white sliced surface. • According to histology, the tumor is made up of bland spindled cells that are expanding within a collagenous stroma.
Ovarian tumors that are borderline epithelial
A class of epithelial tumors known as borderline epithelial ovarian tumors tends to behave indolently yet shows more marked proliferation than benign epithelial tumors. Serous (borderline serous) tumors make up the great bulk of borderline epithelial tumors. At the macroscopic level, they are enormous, often bilateral, cystic tumors that are typically multifocal. Numerous papillary excrescences protrude from the cysts' surface. The tumors exhibit low-grade nuclear atypia and are histologically formed of complicated branching papillae covered by proliferating columnar epithelial cells. The existence of tiny tumor "implants" in the peritoneum or omentum in around 15% to 30% of cases is an odd characteristic of borderline serous tumors. These implants can be classified as either invasive or non-invasive histologically. The majority are non-invasive, and the prognosis for these patients is typically favorable. Although invasive implants are extremely uncommon, they are typically linked to a poor prognosis
- Published on
Pathology - Ovarian carcinomas
Definition: A collection of malignant epithelial tumors originating in the ovary.
Epidemiology • Rare, however a predominant cause of cancer-related mortality owing to its delayed presentation.
Aetiology • High parity and the utilization of oral contraceptives are consistently linked to a diminished risk of ovarian cancer. • Post-menopausal women using oestrogen replacement treatment have an elevated risk. • Emerging evidence indicates that obesity correlates with an increased risk.
Carcinogenesis • Recent morphological and genetic evidence indicates that ovarian carcinomas can be classified into several types based on their probable origin and behavior. One group (low-grade serous, mucinous, Brenner) has indolent behavior and infrequently demonstrates TP53 mutations. Certain workers hypothesize that these tumors originate from paraovarian Müllerian epithelium via a progression from benign cystadenoma to borderline neoplasm to invasive carcinoma. The second category, comprising high-grade serous, high-grade endometrioid, and undifferentiated carcinomas, represents highly aggressive malignancies that often exhibit TP53 mutations. Certain workers hypothesize that these tumors may originate in other pelvic organs, such as the Fallopian tubes, and subsequently affect the ovaries. Endometrioid and clear cell ovarian carcinomas are believed to develop from ovarian endometriosis.
Presentation: stomach pain, tiredness, abdominal distension, and diarrhea. The ambiguous and nonspecific characteristics of the symptoms frequently lead women to attribute them to stress or menopause. Women who pursue medical care are frequently misdiagnosed with benign gastrointestinal or urinary disorders. Most women present with advanced disease at the time of diagnosis. Macroscopy The ovary is hypertrophied and substituted by a neoplastic tumor that is frequently both solid and cystic. Mucinous tumors may comprise gelatinous substances. Histopathology Serous carcinomas consist of malignant epithelial cells that proliferate in irregular branching papillae and create slit-like glandular gaps. Psammoma bodies may be observed.
Endometrioid carcinomas consist of malignant epithelial cells that create round or oval glands similar to those found in endometrial carcinomas. Regions of squamous differentiation are prevalent. Mucinous carcinomas consist of malignant epithelial cells characterized by mucinous cytoplasm that forms glandular structures. Differentiating original ovarian mucinous carcinoma from metastatic mucinous carcinoma originating in the gastrointestinal tract can be quite challenging. transparent cell carcinomas consist of malignant epithelial cells characterized by transparent cytoplasm and hobnailing, which proliferate in tiny tubules and papillae. Transitional cell carcinomas exhibit morphological similarities to urothelial carcinomas; however, their immunophenotypic characteristics align more closely with serous carcinomas.
Prognosis: Generally unfavorable, as the majority of women arrive with advanced disease (FIGO III and IV), correlating with a 5-year survival rate of 25–30% (in contrast to 80–90% for FIGO I or II).
FIGO staging of ovarian carcinomas
IA: tumour limited to one ovary; capsule intact, no tumour on the
ovarian surface; no malignant cells in ascites or peritoneal washings.
IB: tumour limited to both ovaries; capsule intact, no tumour on the
ovarian surface; no malignant cells in ascites or peritoneal washings.
IC: tumour limited to one or both ovaries with any of the following:
capsule ruptured, tumour on the ovarian surface, malignant cells in ascites
or peritoneal washings.
IIA: extension and/or implants on the uterus and/or tube(s); no malignant
cells in ascites or peritoneal washings.
IIB: extension to other pelvic tissues; no malignant cells in ascites or
peritoneal washings.
IIC: pelvic extension with malignant cells in ascites or peritoneal
washings.
IIIA: microscopic peritoneal metastasis beyond the pelvis.
IIIB: macroscopic peritoneal metastasis beyond the pelvis, 2cm or less
in size.
IIIC: peritoneal metastasis beyond the pelvis, > 2cm in size and/or
regional lymph node metastasis.
IV: distant metastasis
Definition: A collection of malignant epithelial tumors originating in the ovary.
Epidemiology • Rare, however a predominant cause of cancer-related mortality owing to its delayed presentation.
Aetiology • High parity and the utilization of oral contraceptives are consistently linked to a diminished risk of ovarian cancer. • Post-menopausal women using oestrogen replacement treatment have an elevated risk. • Emerging evidence indicates that obesity correlates with an increased risk.
Carcinogenesis • Recent morphological and genetic evidence indicates that ovarian carcinomas can be classified into several types based on their probable origin and behavior. One group (low-grade serous, mucinous, Brenner) has indolent behavior and infrequently demonstrates TP53 mutations. Certain workers hypothesize that these tumors originate from paraovarian Müllerian epithelium via a progression from benign cystadenoma to borderline neoplasm to invasive carcinoma. The second category, comprising high-grade serous, high-grade endometrioid, and undifferentiated carcinomas, represents highly aggressive malignancies that often exhibit TP53 mutations. Certain workers hypothesize that these tumors may originate in other pelvic organs, such as the Fallopian tubes, and subsequently affect the ovaries. Endometrioid and clear cell ovarian carcinomas are believed to develop from ovarian endometriosis.
Presentation: stomach pain, tiredness, abdominal distension, and diarrhea. The ambiguous and nonspecific characteristics of the symptoms frequently lead women to attribute them to stress or menopause. Women who pursue medical care are frequently misdiagnosed with benign gastrointestinal or urinary disorders. Most women present with advanced disease at the time of diagnosis. Macroscopy The ovary is hypertrophied and substituted by a neoplastic tumor that is frequently both solid and cystic. Mucinous tumors may comprise gelatinous substances. Histopathology Serous carcinomas consist of malignant epithelial cells that proliferate in irregular branching papillae and create slit-like glandular gaps. Psammoma bodies may be observed.
Endometrioid carcinomas consist of malignant epithelial cells that create round or oval glands similar to those found in endometrial carcinomas. Regions of squamous differentiation are prevalent. Mucinous carcinomas consist of malignant epithelial cells characterized by mucinous cytoplasm that forms glandular structures. Differentiating original ovarian mucinous carcinoma from metastatic mucinous carcinoma originating in the gastrointestinal tract can be quite challenging. transparent cell carcinomas consist of malignant epithelial cells characterized by transparent cytoplasm and hobnailing, which proliferate in tiny tubules and papillae. Transitional cell carcinomas exhibit morphological similarities to urothelial carcinomas; however, their immunophenotypic characteristics align more closely with serous carcinomas.
Prognosis: Generally unfavorable, as the majority of women arrive with advanced disease (FIGO III and IV), correlating with a 5-year survival rate of 25–30% (in contrast to 80–90% for FIGO I or II).
FIGO staging of ovarian carcinomas
IA: tumour limited to one ovary; capsule intact, no tumour on the
ovarian surface; no malignant cells in ascites or peritoneal washings.
IB: tumour limited to both ovaries; capsule intact, no tumour on the
ovarian surface; no malignant cells in ascites or peritoneal washings.
IC: tumour limited to one or both ovaries with any of the following:
capsule ruptured, tumour on the ovarian surface, malignant cells in ascites
or peritoneal washings.
IIA: extension and/or implants on the uterus and/or tube(s); no malignant
cells in ascites or peritoneal washings.
IIB: extension to other pelvic tissues; no malignant cells in ascites or
peritoneal washings.
IIC: pelvic extension with malignant cells in ascites or peritoneal
washings.
IIIA: microscopic peritoneal metastasis beyond the pelvis.
IIIB: macroscopic peritoneal metastasis beyond the pelvis, 2cm or less
in size.
IIIC: peritoneal metastasis beyond the pelvis, > 2cm in size and/or
regional lymph node metastasis.
IV: distant metastasis
- Published on
Pathology - Pelvic inflammatory disease
Definition: An infection of the upper female vaginal canal.
Epidemiology • The majority of instances occur in young sexually active women aged 15 to 25. The true incidence is challenging to ascertain due to numerous undiagnosed instances.
Aetiology • The majority of cases result from ascending infections caused by either Chlamydia (C.) trachomatis or Neisseria (N.) gonorrhoeae. Both organisms are sexually transmitted microorganisms. • Cases not linked to sexually transmitted infections are frequently connected with intrauterine devices or retained products of conception following childbirth or miscarriage.
Presentation • Typically, there are enduring symptoms of pelvic discomfort, dyspareunia, and post-coital or intermenstrual bleeding. • Severe instances may result in an acute illness characterized by fever, abdominal pain, and peritonitis. 2 It is important to recognize that numerous women remain asymptomatic and consequently undetected.
Complications • Infertility: the likelihood of infertility escalates with each occurrence of infection. Women who experience three or more bouts of pelvic inflammatory disease (PID) have a 40% likelihood of infertility. • Ectopic pregnancy: the chance is increased sixfold, perhaps due to deformation and scarring of the fallopian tubes. • Persistent pelvic pain and painful intercourse
Definition: An infection of the upper female vaginal canal.
Epidemiology • The majority of instances occur in young sexually active women aged 15 to 25. The true incidence is challenging to ascertain due to numerous undiagnosed instances.
Aetiology • The majority of cases result from ascending infections caused by either Chlamydia (C.) trachomatis or Neisseria (N.) gonorrhoeae. Both organisms are sexually transmitted microorganisms. • Cases not linked to sexually transmitted infections are frequently connected with intrauterine devices or retained products of conception following childbirth or miscarriage.
Presentation • Typically, there are enduring symptoms of pelvic discomfort, dyspareunia, and post-coital or intermenstrual bleeding. • Severe instances may result in an acute illness characterized by fever, abdominal pain, and peritonitis. 2 It is important to recognize that numerous women remain asymptomatic and consequently undetected.
Complications • Infertility: the likelihood of infertility escalates with each occurrence of infection. Women who experience three or more bouts of pelvic inflammatory disease (PID) have a 40% likelihood of infertility. • Ectopic pregnancy: the chance is increased sixfold, perhaps due to deformation and scarring of the fallopian tubes. • Persistent pelvic pain and painful intercourse
- Published on
Pathology - Cervical carcinoma
Definition • A malignant epithelial neoplasm originating in the cervix.
Epidemiology • Globally, cervical carcinoma represents the predominant malignancy of the female genital tract and the second most prevalent non-cutaneous malignancy in women, following breast cancer. • In developed nations, cervical carcinoma ranks as the third most common malignancy of the female genital tract, subsequent to endometrial and ovarian carcinoma. The reduced incidence is primarily due to the effectiveness of cervical screening programs.
Aetiology: Nearly all cases are attributable to high-risk HPV infection, specifically strains 16 and 18. Other risk factors encompass smoking and the use of oral contraceptives, perhaps contributing to the persistence of HPV in the cervix. Carcinogenesis: 80% of cases are squamous cell carcinomas originating from a precursor lesion termed cervical intraepithelial neoplasia (CIN). Twenty percent are adenocarcinomas that originate from a precursor lesion termed cervical glandular intraepithelial neoplasia (CGIN). HPV-induced cervical carcinogenesis is associated with the expression of two viral genes, E6 and E7. The E6 and E7 proteins interact with the tumor suppressor proteins, P53 and RB, facilitating their destruction. The dysfunction of these proteins leads to unregulated growth of the infected cells.
Presentation: Non-menstrual vaginal hemorrhage and secretion. Macroscopy • Observable tumors present as a solid mass on the cervix, which may exhibit exophytic or endophytic growth patterns.
Histopathology • Squamous cell carcinomas are distinguished by infiltrating irregular nests of malignant epithelial cells demonstrating squamous differentiation. Residual CIN may be observed next to diminutive tumors. Adenocarcinomas are defined by the infiltration of malignant epithelial cells that create glandular structures. Residual CGIN may be observed close to diminutive tumors.
Prognosis is contingent upon several criteria, including age, stage, and the presence or absence of lymphovascular invasion.
FIGO staging of cervical carcinomas
IA1: microscopic tumour with stromal invasion d 3mm in depth, d 7mm
in horizontal spread.
IA2: microscopic tumour with stromal invasion > 3mm in depth and not
more than 5mm with a horizontal spread d 7mm.
IB: any clinically visible lesion confi ned to the cervix or microscopic
lesion greater than IA1/2.
II: tumour invades beyond the uterus, but not to the pelvic side wall or
to the lower third of the vagina.
IIIA: tumour involves the lower third of vagina, no extension to the
pelvic side wall.
IIIB: tumour extends to the pelvic side wall and/or causes hydronephrosis
or non-functioning kidney.
IVA: tumour invades the mucosa of bladder or rectum and/or extends
beyond the true pelvis.
IVB: distant metastasis
Definition • A malignant epithelial neoplasm originating in the cervix.
Epidemiology • Globally, cervical carcinoma represents the predominant malignancy of the female genital tract and the second most prevalent non-cutaneous malignancy in women, following breast cancer. • In developed nations, cervical carcinoma ranks as the third most common malignancy of the female genital tract, subsequent to endometrial and ovarian carcinoma. The reduced incidence is primarily due to the effectiveness of cervical screening programs.
Aetiology: Nearly all cases are attributable to high-risk HPV infection, specifically strains 16 and 18. Other risk factors encompass smoking and the use of oral contraceptives, perhaps contributing to the persistence of HPV in the cervix. Carcinogenesis: 80% of cases are squamous cell carcinomas originating from a precursor lesion termed cervical intraepithelial neoplasia (CIN). Twenty percent are adenocarcinomas that originate from a precursor lesion termed cervical glandular intraepithelial neoplasia (CGIN). HPV-induced cervical carcinogenesis is associated with the expression of two viral genes, E6 and E7. The E6 and E7 proteins interact with the tumor suppressor proteins, P53 and RB, facilitating their destruction. The dysfunction of these proteins leads to unregulated growth of the infected cells.
Presentation: Non-menstrual vaginal hemorrhage and secretion. Macroscopy • Observable tumors present as a solid mass on the cervix, which may exhibit exophytic or endophytic growth patterns.
Histopathology • Squamous cell carcinomas are distinguished by infiltrating irregular nests of malignant epithelial cells demonstrating squamous differentiation. Residual CIN may be observed next to diminutive tumors. Adenocarcinomas are defined by the infiltration of malignant epithelial cells that create glandular structures. Residual CGIN may be observed close to diminutive tumors.
Prognosis is contingent upon several criteria, including age, stage, and the presence or absence of lymphovascular invasion.
FIGO staging of cervical carcinomas
IA1: microscopic tumour with stromal invasion d 3mm in depth, d 7mm
in horizontal spread.
IA2: microscopic tumour with stromal invasion > 3mm in depth and not
more than 5mm with a horizontal spread d 7mm.
IB: any clinically visible lesion confi ned to the cervix or microscopic
lesion greater than IA1/2.
II: tumour invades beyond the uterus, but not to the pelvic side wall or
to the lower third of the vagina.
IIIA: tumour involves the lower third of vagina, no extension to the
pelvic side wall.
IIIB: tumour extends to the pelvic side wall and/or causes hydronephrosis
or non-functioning kidney.
IVA: tumour invades the mucosa of bladder or rectum and/or extends
beyond the true pelvis.
IVB: distant metastasis
- Published on
Pathology - Endometrial carcinoma
Definition: A malignant epithelial tumor originating in the endometrium.
Epidemiology • The predominant malignant neoplasm of the female reproductive system in civilized nations. • 85% are estrogen-dependent ('type 1') tumors, prevalent in women in their 50s and 60s. • 15% are estrogen-independent ('type 2') tumors, observed in older women in their 70s and 80s.
Aetiology • Oestrogen-dependent neoplasms are linked to diabetes, obesity, nulliparity, early menarche, late menopause, and polycystic ovarian syndrome. The etiology of estrogen-independent tumors is less defined.
Carcinogenesis • Estrogen-dependent tumors arise from a precursor lesion known as endometrial intraepithelial neoplasia (atypical hyperplasia) against a backdrop of (simple) endometrial hyperplasia. The loss of PTEN function is characteristic. • Oestrogen-independent tumors arise from a precursor lesion known as endometrial intraepithelial carcinoma against a backdrop of endometrial atrophy. The dysfunction of the TP53 gene is characteristic.
Presentation • The primary symptom is post-menopausal hemorrhage. Macroscopy • An exophytic, friable mass occupies the endometrial cavity and infiltrates to variable degrees into the underlying myometrium. • In advanced cases, the tumor may penetrate the serosal surface or infect the cervix.
Histopathology • Estrogen-dependent tumors are typically well-differentiated endometrioid adenocarcinomas characterized by malignant epithelial cells that create intricate villoglandular formations. Oestrogen-independent tumors are typically serous carcinomas or clear cell carcinomas, which closely resemble their ovarian equivalents. Both are high-grade neoplasms with widespread dissemination at the time of presentation.
Prognosis: Oestrogen-dependent tumors typically have a favorable prognosis. Oestrogen-independent tumors exhibit great aggressiveness and are typically lethal.
Definition: A malignant epithelial tumor originating in the endometrium.
Epidemiology • The predominant malignant neoplasm of the female reproductive system in civilized nations. • 85% are estrogen-dependent ('type 1') tumors, prevalent in women in their 50s and 60s. • 15% are estrogen-independent ('type 2') tumors, observed in older women in their 70s and 80s.
Aetiology • Oestrogen-dependent neoplasms are linked to diabetes, obesity, nulliparity, early menarche, late menopause, and polycystic ovarian syndrome. The etiology of estrogen-independent tumors is less defined.
Carcinogenesis • Estrogen-dependent tumors arise from a precursor lesion known as endometrial intraepithelial neoplasia (atypical hyperplasia) against a backdrop of (simple) endometrial hyperplasia. The loss of PTEN function is characteristic. • Oestrogen-independent tumors arise from a precursor lesion known as endometrial intraepithelial carcinoma against a backdrop of endometrial atrophy. The dysfunction of the TP53 gene is characteristic.
Presentation • The primary symptom is post-menopausal hemorrhage. Macroscopy • An exophytic, friable mass occupies the endometrial cavity and infiltrates to variable degrees into the underlying myometrium. • In advanced cases, the tumor may penetrate the serosal surface or infect the cervix.
Histopathology • Estrogen-dependent tumors are typically well-differentiated endometrioid adenocarcinomas characterized by malignant epithelial cells that create intricate villoglandular formations. Oestrogen-independent tumors are typically serous carcinomas or clear cell carcinomas, which closely resemble their ovarian equivalents. Both are high-grade neoplasms with widespread dissemination at the time of presentation.
Prognosis: Oestrogen-dependent tumors typically have a favorable prognosis. Oestrogen-independent tumors exhibit great aggressiveness and are typically lethal.
- Published on
Pathology - hydatidiform Moles
Definition: An aberrant proliferation of trophoblasts is a hallmark of a particular type of gestational trophoblastic illness. There are two kinds of moles: partial moles and complete moles. The study of epidemiology In the western world, about one out of every 1000 pregnancies is molar. In regions of the Far East, where incidence rates might reach 1 in 80, they are far more prevalent for unclear reasons. Genetics: All chromosomes in whole moles are derived from their fathers, and they are often diploid (46 XX or 46 XY). Partial moles are triploid (69 XXY, 69 XXX, or 69 XYY) with one set of mother chromosomes and two sets of paternal chromosomes. They develop when a haploid sperm fertilizes an anucleate ovum, then copies its genetic material. They are produced when two sperm fertilize an ovum. Presentation: The majority have an early miscarriage. Typically, molar pregnancy is diagnosed after a histological analysis of the removed products of conception; there is no clinical suspicion of molar pregnancy. The majority of molar products of conception are quite ordinary in terms of macroscopy. • Villi that are clearly hydropic may be seen in cases that appear late.
Histopathology • Villi with a distinctive lobulated "budding" architecture are seen in whole moles. The myxoid stroma of the villi contains karyorrhectic debris and collapsed empty blood vessels. Sheets of pleomorphic extravillous trophoblast may be present, along with aberrant non-polar trophoblastic hyperplasia. A noticeable implantation site reaction is frequently observed, although the typical trophoblast blockage of multiple blood arteries is absent. Villi with uneven, "dentate," or "geographic" contours are detected in partial moles. Villous blood arteries containing nucleated fetal red blood cells and noticeable villous pseudo-inclusions are present in the frequently fibrotic villi. There is abnormal non-polar trophoblastic hyperplasia, although it is typically localized and less noticeable than in whole moles. With typical trophoblast blockage of decidual blood arteries, the implantation site is typically inconspicuous.
Prognosis: B HCG levels quickly return to normal after molar tissue evacuation, which is typically curative. Persistent prenatal trophoblastic illness, which complicates around 15% of full moles and 1% of partial moles and necessitates chemotherapy to cure, is indicated by persistent B HCG levels.
Choriocarcinoma during pregnancy
Choriocarcinoma is an uncommon but extremely dangerous trophoblastic tumor that is another kind of prenatal trophoblastic illness. Half of them arise from a previous hydatidiform mole, whereas the other half happen after a non-molar miscarriage or a normal pregnancy. According to histology, choriocarcinomas are made up of a combination of syncytiotrophoblast and cytotrophoblast, which usually form bilaminar structures. Chorionic villi are by definition missing. Due to their high tendency for vascular invasion, choriocarcinomas can spread quickly to several distant locations. Thankfully, most women have a fairly excellent prognosis and pregnant choriocarcinomas react very well to chemotherapy.
Definition: An aberrant proliferation of trophoblasts is a hallmark of a particular type of gestational trophoblastic illness. There are two kinds of moles: partial moles and complete moles. The study of epidemiology In the western world, about one out of every 1000 pregnancies is molar. In regions of the Far East, where incidence rates might reach 1 in 80, they are far more prevalent for unclear reasons. Genetics: All chromosomes in whole moles are derived from their fathers, and they are often diploid (46 XX or 46 XY). Partial moles are triploid (69 XXY, 69 XXX, or 69 XYY) with one set of mother chromosomes and two sets of paternal chromosomes. They develop when a haploid sperm fertilizes an anucleate ovum, then copies its genetic material. They are produced when two sperm fertilize an ovum. Presentation: The majority have an early miscarriage. Typically, molar pregnancy is diagnosed after a histological analysis of the removed products of conception; there is no clinical suspicion of molar pregnancy. The majority of molar products of conception are quite ordinary in terms of macroscopy. • Villi that are clearly hydropic may be seen in cases that appear late.
Histopathology • Villi with a distinctive lobulated "budding" architecture are seen in whole moles. The myxoid stroma of the villi contains karyorrhectic debris and collapsed empty blood vessels. Sheets of pleomorphic extravillous trophoblast may be present, along with aberrant non-polar trophoblastic hyperplasia. A noticeable implantation site reaction is frequently observed, although the typical trophoblast blockage of multiple blood arteries is absent. Villi with uneven, "dentate," or "geographic" contours are detected in partial moles. Villous blood arteries containing nucleated fetal red blood cells and noticeable villous pseudo-inclusions are present in the frequently fibrotic villi. There is abnormal non-polar trophoblastic hyperplasia, although it is typically localized and less noticeable than in whole moles. With typical trophoblast blockage of decidual blood arteries, the implantation site is typically inconspicuous.
Prognosis: B HCG levels quickly return to normal after molar tissue evacuation, which is typically curative. Persistent prenatal trophoblastic illness, which complicates around 15% of full moles and 1% of partial moles and necessitates chemotherapy to cure, is indicated by persistent B HCG levels.
Choriocarcinoma during pregnancy
Choriocarcinoma is an uncommon but extremely dangerous trophoblastic tumor that is another kind of prenatal trophoblastic illness. Half of them arise from a previous hydatidiform mole, whereas the other half happen after a non-molar miscarriage or a normal pregnancy. According to histology, choriocarcinomas are made up of a combination of syncytiotrophoblast and cytotrophoblast, which usually form bilaminar structures. Chorionic villi are by definition missing. Due to their high tendency for vascular invasion, choriocarcinomas can spread quickly to several distant locations. Thankfully, most women have a fairly excellent prognosis and pregnant choriocarcinomas react very well to chemotherapy.
- Published on
Pathology – Endometriosis
Definition • The existence of endometrial tissue outside the confines of the uterine cavity. The majority of cases arise within the pelvis, predominantly affecting the ovaries, uterine sacral ligaments, pelvic peritoneum, pouch of Douglas, and sigmoid colon. Endometriosis is also identified in locations beyond the pelvis, including surgical scars and the lungs, but this occurrence is less common.
Epidemiology • Prevalent, impacting up to 10% of women.
Pathogenesis Implantation theory posits that endometrial glands are expelled into the peritoneal cavity during menstruation and subsequently adhere to the peritoneal surface. This notion is supported by experiments that induce endometriosis in animals through the placement of endometrial tissue in the peritoneal cavity.
The metaplastic theory states that endometriosis develops from the metaplasia of the peritoneal surface epithelium into endometrial-type epithelium. Considering that the peritoneum and female genital tract originate from same embryological cells (coelomic epithelium), this is feasible and would explain the presence of endometriotic deposits in regions where implantation is improbable. The metastatic theory posits that endometriosis develops from the hematogenous dissemination of endometrial tissue that enters the bloodstream during menstruation. This would explain instances occurring in areas where implantation and metaplasia are unlikely, such as the lung.
Presentation: Dysmenorrhea resulting from the inflammation of endometriotic lesions during menstruation. • Subfertility due to ambiguous mechanisms, with implantation failure and/or endocrine disruption suggested as potential causes. There is scant evidence to substantiate tubal distortion as a causative factor in the majority of women.
Macroscopy • Ovarian involvement generally results in cysts with dark brown altered blood, referred to as 'chocolate cysts.' Peritoneal involvement results in tiny nodules that frequently manifest as brown or black.
Histopathology • Microscopic examination is diagnostic, revealing the presence of endometrial glands and endometrial stromal cells in tissues beyond the uterine body. Surrounding hemorrhage is frequently copious.
Prognosis: Endometriosis is chronic and progressive in 50% of instances. Ovarian endometriosis is considered a precursor to ovarian endometrioid carcinomas.
Definition • The existence of endometrial tissue outside the confines of the uterine cavity. The majority of cases arise within the pelvis, predominantly affecting the ovaries, uterine sacral ligaments, pelvic peritoneum, pouch of Douglas, and sigmoid colon. Endometriosis is also identified in locations beyond the pelvis, including surgical scars and the lungs, but this occurrence is less common.
Epidemiology • Prevalent, impacting up to 10% of women.
Pathogenesis Implantation theory posits that endometrial glands are expelled into the peritoneal cavity during menstruation and subsequently adhere to the peritoneal surface. This notion is supported by experiments that induce endometriosis in animals through the placement of endometrial tissue in the peritoneal cavity.
The metaplastic theory states that endometriosis develops from the metaplasia of the peritoneal surface epithelium into endometrial-type epithelium. Considering that the peritoneum and female genital tract originate from same embryological cells (coelomic epithelium), this is feasible and would explain the presence of endometriotic deposits in regions where implantation is improbable. The metastatic theory posits that endometriosis develops from the hematogenous dissemination of endometrial tissue that enters the bloodstream during menstruation. This would explain instances occurring in areas where implantation and metaplasia are unlikely, such as the lung.
Presentation: Dysmenorrhea resulting from the inflammation of endometriotic lesions during menstruation. • Subfertility due to ambiguous mechanisms, with implantation failure and/or endocrine disruption suggested as potential causes. There is scant evidence to substantiate tubal distortion as a causative factor in the majority of women.
Macroscopy • Ovarian involvement generally results in cysts with dark brown altered blood, referred to as 'chocolate cysts.' Peritoneal involvement results in tiny nodules that frequently manifest as brown or black.
Histopathology • Microscopic examination is diagnostic, revealing the presence of endometrial glands and endometrial stromal cells in tissues beyond the uterine body. Surrounding hemorrhage is frequently copious.
Prognosis: Endometriosis is chronic and progressive in 50% of instances. Ovarian endometriosis is considered a precursor to ovarian endometrioid carcinomas.
