Reproductive + pregnancy Flashcards
T135 What is hypospadias?
Hypospadias is an abnormal opening of the urethra on the ventral aspect of the penis, anywhere along the shaft.
Results from incomplete closure of the urethral folds of the urogenital sinus.
Can cause urinary tract obstruction and increased risk of UTIs.
Often associated with other congenital anomalies like inguinal hernia and undescended testicles.
What is epispadias?
Epispadias is an abnormal urethral orifice on the dorsal aspect of the penis.
It is less common than hypospadias.
What is phimosis?
Phimosis is a condition where the foreskin of the penis cannot be pulled back past the glans.
Can result in pain during an erection and increases the risk of balanitis and other complications.
May be congenital or acquired due to scarring from previous episodes of balanoposthitis.
What are balanitis and balanoposthitis?
Balanitis: Inflammation of the glans penis.
Balanoposthitis: Inflammation of both the glans and the overlying prepuce.
Often caused by poor hygiene and accumulation of smegma.
Common causative agents include Candida albicans, anaerobic bacteria, Gardnerella, and pyogenic bacteria.
What is squamous cell carcinoma of the penis?
Squamous cell carcinoma accounts for more than 95% of penile neoplasms.
Common in the glans or shaft of the penis as ulcerated, infiltrative lesions.
Increased risk in uncircumcised males over 40.
Risk factors include HPV serotypes 16 and 18, poor hygiene, and smoking.
What is Bowen disease in the context of penile cancer?
Bowen disease is squamous cell carcinoma in situ of the penis.
Appears as a solitary plaque on the shaft of the penis in older, uncircumcised males.
Histologically, it shows dysplasia with several mitotic figures, dyskeratosis, and nuclear pleomorphism above an intact basement membrane.
Describe invasive squamous cell carcinoma of the penis.
Appears as a gray, crusted, papular lesion, often on the glans penis or prepuce.
Infiltration of underlying connective tissue produces an ulcerated lesion with irregular margins.
Histologically, it is a typical keratinizing squamous cell carcinoma.
Prognosis is related to the tumor stage and it may metastasize to inguinal lymph nodes.
What is verrucous carcinoma of the penis?
A variant of squamous cell carcinoma characterized by a papillary architecture and virtually no cytologic atypia.
Features rounded, pushing deep margins.
Locally invasive but does not metastasize.
T136 What is a hydrocele?
Hydrocele is the accumulation of serous fluid within the tunica vaginalis (the serous membrane covering the testicle and internal surface of the scrotum).
Causes of hydrocele
Causes include:
Neighboring infection.
Tumor or blockage of lymphatic drainage (e.g., chyloceles in elephantiasis in adults).
Idiopathic.
Incomplete closure of the processus vaginalis, leading to communication with the peritoneal cavity (common in infants).
It can be distinguished from other fluid collections like blood, pus, or lymph by its ability to allow light to pass through (transillumination).
What is a hematocele?
Hematocele is the accumulation of blood in the tunica vaginalis.
What are the common causes of nonspecific epididymitis?
Usually due to primary UTI spreading to testis.
Pathogens: E. coli, pseudomonas.
Testis is swollen, tender, and contains neutrophils.
What are the typical pathogens in epididymitis in young adults?
Chlamydia trachomatis (serotypes D-K).
Neisseria gonorrhoeae.
What are the features of mumps orchitis?
Orchitis occurs in ~20% of infected adult males.
Testis is edematous, congested, with lymphoplasmacytic infiltrate.
Severe infection: necrosis, seminiferous epithelium loss, atrophy, fibrosis, sterility.
Describe the histology of testicular tuberculosis.
Begins as epididymitis, then involves testis.
Granulomatous inflammation and caseous necrosis.
What is autoimmune orchitis?
Characterized by granulomas involving seminiferous tubules.
What happens during testicular torsion?
Twisting of the spermatic cord.
Thin-walled veins obstructed, causing congestion and hemorrhagic infarction.
Intense vascular engorgement and venous infarction follow if not relieved.
What are the two types of testicular torsion?
Neonatal torsion: Occurs in utero or shortly after birth.
Adult torsion: Typically seen in adolescence with sudden onset pain, often due to bilateral anatomic defect (bell clapper anomaly).
What is the bell clapper anomaly?
Anatomic defect where the testis lacks posterior adherence to the inner wall of the scrotum.
Increased testicular mobility, leading to torsion.
What is a varicocele?
Dilation of the spermatic vein due to impaired drainage.
Presents as scrotal swelling with dilated veins appearance.
Commonly left-sided; associated with left-sided renal cell carcinoma.
Seen in many infertile males.
Why is varicocele usually left-sided?
Left testicular vein drains into the left renal vein.
Right testicular vein drains directly into the IVC.
Left-sided renal cell carcinoma can invade the renal vein.
What is cryptorchidism?
Failure of one or both testes to descend.
Normally, testes descend from the abdominal cavity into the pelvis by the third month and then through the inguinal canal into the scrotum during the last 2 months of intrauterine life.
When is cryptorchidism diagnosed and treated?
Diagnosis typically established at age 1 in ~1% of male babies.
Most cases resolve spontaneously.Orchiopexy is performed before age 2 if not resolved.
Where are undescended testes most commonly found in cryptorchidism?
Most commonly found in the inguinal canal.
What happens to undescended testes over time in cryptorchidism?
Testes become atrophic.
Tubular atrophy evident by age 5-6.
Hyalinization present by puberty.
Foci of intratubular germ cell neoplasia may be present.
What are the risks associated with cryptorchidism?
Increased risk of infertility.
Increased risk of developing testicular cancer, affecting both testes even in unilateral cases.
T137 What are the two major groups of testicular neoplasms?
- Germ cell tumors - ~95% of cases, all malignant, usually occur between ages 15-40.
- Sex cord-stromal tumors (Sertoli or Leydig cells) - uncommon, usually benign.
What are the risk factors for testicular neoplasms?
Cryptorchidism (3-5 fold increase).
Testicular dysgenesis (e.g., testicular feminization and Klinefelter syndrome).
Caucasians > African Americans.
Family history.
Isochromosome of the short arm of chromosome 12 in germ cell tumors.
What lesion is found in most testicular tumors in post-pubertal males?
Intratubular germ cell neoplasm (in-situ lesion).
What is the clinical presentation of testicular neoplasms?
Firm, painless testicular mass
What are the characteristics of seminomas?
Account for 50% of testicular neoplasms.
Remain confined to the testis for a long time.
Spread mainly to para-aortic nodes.
Distant spread is rare.
What are the characteristics of non-seminomatous testicular tumors?
Tend to spread earlier by both lymph and blood vessels.
What is the treatment for testicular neoplasms?
Radical orchiectomy and chemotherapy.
What are the characteristics of germ cell tumors in terms of composition?
60% of germ cell tumors are mixed and contain more than one component, arising from pluripotent neoplastic germ cells.
What is the most common type of testicular cancer and its prognosis?
Seminoma.
Good prognosis with late metastasis and responsiveness to treatment.
Describe the gross appearance of a seminoma.
Soft, well-demarcated, gray-white tumor.
Homogenous cut surface with no hemorrhage or necrosis.
Describe the microscopic appearance of a seminoma.
Large polygonal, uniform cells with distinct borders.
Clear, glycogen-rich cytoplasm.
Round nuclei and visible nucleoli.
Arranged in small lobules separated by fibrous septae with possible lymphocytic infiltrate.
What is a variant of seminoma and its characteristics?
Spermatocytic seminoma.
Affects older men.
Lacks lymphocytic infiltrate and syncytiotrophoblasts.
Not associated with intralobular germ cell neoplasm and does not metastasize.
What is the significance of syncytiotrophoblasts in seminomas?
Present in 10% of cases.
Source of minimally elevated serum hCG concentration.
What are the characteristics of embryonal carcinoma?
Rare (2-3%).
Poor prognosis with early metastasis and poor reaction to treatment.
Common in ages 20-30.
Malignant tumor with immature, primitive cells.
Gross: Mass with hemorrhage and necrosis.
Micro: Large primitive cells with basophilic cytoplasm, indistinct borders, and large hyperchromatic nuclei with prominent nucleoli.
Tumor markers: Negative for pure embryonal carcinoma but can show markers if mixed with choriocarcinoma or yolk sac tumor cells.
What are the gross and microscopic features of embryonal carcinoma?
Gross: Mass with hemorrhage and necrosis.
Micro: Large primitive cells with basophilic cytoplasm, indistinct borders, large hyperchromatic nuclei with prominent nucleoli, and pleomorphic cells in cords, sheets, or gland-like arrangements.
Describe the characteristics of choriocarcinoma.
Highly malignant with early hematogenous metastases, commonly to liver and lung.
Common in ages 20-30.
Tumor comprised of trophoblastic (placenta-forming) cells.
Gross: Often small, non-palpable lesions with hemorrhage.
Micro: Proliferation of syncytiotrophoblasts (large eosinophilic multinucleated cells) and cuboidal cytotrophoblasts.
Tumor marker: hCG.
What are the gross and microscopic features of choriocarcinoma?
Gross: Small, non-palpable lesions with hemorrhage on cut surface.
Micro: Syncytiotrophoblasts (large eosinophilic multinucleated cells) intermingle with small cuboidal cytotrophoblasts.
What is the significance of tumor markers in embryonal carcinoma and choriocarcinoma?
Embryonal carcinoma: Negative for pure form, but mixed tumors may show markers from choriocarcinoma or yolk sac tumors.
Choriocarcinoma: hCG is a significant marker.
What is the yolk sac tumor (endodermal sinus tumor)?
Most common germ cell tumor in children younger than 3.
Good prognosis in children.In adults, often mixed with embryonic carcinoma.
Tumor marker: alpha-fetoprotein (AFP).
What are the gross and microscopic features of yolk sac tumor (endodermal sinus tumor)?
Macro: Large and may be well demarcated.
Micro: Low cuboidal to columnar epithelial cells forming microcysts and lace-like (reticular) patterns.
Schiller-Duval bodies (resemble developing glomeruli) are characteristic.
What is the significance of tumor markers in yolk sac tumor (endodermal sinus tumor)?
Alpha-fetoprotein (AFP) is a significant marker for yolk sac tumors.
What are Schiller-Duval bodies?
Schiller-Duval bodies are structures resembling developing glomeruli and are characteristic of yolk sac tumors (endodermal sinus tumors).
What is a teratoma?
A germ cell tumor with neoplastic cells differentiating along somatic cell lines.
Majority are malignant in males and benign in females.
Contains tissues from two or three embryonic layers (ectoderm, endoderm, and mesoderm).
What is a teratoma?
A germ cell tumor with neoplastic cells differentiating along somatic cell lines.
Majority are malignant in males and benign in females.
Contains tissues from two or three embryonic layers (ectoderm, endoderm, and mesoderm).
What are the gross and microscopic features of a teratoma?
Gross: Often cystic masses that may contain cartilage.
Micro: Composed of mature fetal tissue derived from multiple embryonic layers in a haphazard arrangement (e.g., cartilage, neural tissue, glandular/squamous epithelium).
At what age are teratomas more common and what is their malignancy status?
More common and benign in young age.
Rare and malignant in older age.
Rarely, non-germ cell tumors may arise in teratoma (teratoma with malignant transformation).
What are the tumor markers associated with teratomas?
90% of patients have elevated hCG and AFP.
What is the yolk sac tumor (endodermal sinus tumor)?
Most common germ cell tumor in children younger than 3.
Good prognosis in children.
In adults, often mixed with embryonic carcinoma.
Tumor marker: alpha-fetoprotein (AFP).
What are the gross and microscopic features of yolk sac tumor (endodermal sinus tumor)?
Macro: Large and may be well demarcated.
Micro: Low cuboidal to columnar epithelial cells forming microcysts and lace-like (reticular) patterns.
Schiller-Duval bodies (resemble developing glomeruli) are characteristic.
What is the significance of tumor markers in yolk sac tumor (endodermal sinus tumor)?
Alpha-fetoprotein (AFP) is a significant marker for yolk sac tumors.
What are Schiller-Duval bodies?
Schiller-Duval bodies are structures resembling developing glomeruli and are characteristic of yolk sac tumors (endodermal sinus tumors).
T138 Describe the location and anatomical divisions of the prostate gland.
Lies at the base of the bladder, encircling the urethra (prostatic urethra).
Sits anterior to the rectum; posterior aspect palpable by digital rectal exam.
Divided into peripheral and transition zones: hyperplastic lesions common in transition zone; carcinoma common in peripheral zone.
What is the histological structure of the normal prostate gland?
Contains glands with two cell layers: a flat basal layer and an overlying columnar secretory cell layer.
Surrounding prostatic stroma contains a mixture of smooth muscle and fibrous tissue.
What is the primary function of the prostate gland?
Secretes an alkaline, milky fluid that is added to sperm and seminal vesicle fluid to make semen.
How are the glands and stroma of the prostate maintained?
Maintained by androgens.
Predominantly regulated by dihydrotestosterone (DHT), a metabolite of testosterone.
What are the four categories of inflammation of the prostate?
Acute bacterial prostatitis.
Chronic bacterial prostatitis.
Chronic prostatitis / chronic pelvic pain syndrome.
Granulomatous prostatitis.
What are the clinical features and common pathogens of acute bacterial prostatitis?
Acute infiltrate seen in prostatic acini and stroma.
Clinically associated with fever, chills, and dysuria.
Rectal examination: prostate is tender.
Common pathogens: Chlamydia and Gonorrhea in young men; E. coli in older men.
What are the features of chronic bacterial prostatitis?
Associated with recurrent UTI.Presents as dysuria with pelvic or low back pain.
Culture may come negative, but prostate shows infiltrate of lymphocytes, plasma cells, and macrophages.
What characterizes chronic nonbacterial prostatitis or chronic pelvic pain syndrome?
Difficult to diagnose.
Clinically similar to chronic bacterial prostatitis with persistent pain, especially after ejaculation.
No bacteria cultured from expressed prostatic secretions.
Excessive white blood cells (WBC) may be present or absent.
Describe granulomatous prostatitis and its common causes.
An inflammatory condition of the prostate with granulomas.
Most common cause: instillation of Bacillus Calmette-Guérin (BCG) for bladder cancer treatment.
Histologically indistinguishable from tuberculosis.
Fungal granulomatous prostatitis seen in immunocompromised hosts.
Nonspecific granulomatous prostatitis is a reaction to secretions from ruptured prostatic ducts and acini.
What is benign prostate hyperplasia (BPH) and how common is it?
Benign proliferation of stromal and epithelial elements, not leading to cancer.
Very common, starts at age 40, and affects 90% of men by age 80.
Describe the pathogenesis of benign prostate hyperplasia.
Excessive androgen-dependent growth/trophic glandular hyperplasia.
Central role of Dihydrotestosterone (DHT) synthesized in the prostate from circulating testosterone by enzyme 5α-reductase.
DHT binds to nuclear androgen receptors, regulating gene expression for growth and survival of prostatic epithelium and stromal cells.
What is the morphology of benign prostate hyperplasia?
Occurs in the inner, transitional zone of the prostate.
Enlarged prostate with well-demarcated nodules; nodules may be solid or contain cystic spaces.
Adenomatous nodules composed of proliferating fibromuscular stroma surrounding proliferated glandular epithelium, maintaining distinct basal and tall columnar layers.
Nodules create papillary infolding into cystic lumens containing proteinaceous secretory material (Corpora Amylacea).
What are the clinical symptoms of benign prostate hyperplasia?
Lower urinary tract obstruction in only 10% of men.
Difficulty starting urine stream and intermittent interruptions.
Presence of residual urine in the bladder increases the risk of UTI.
Symptoms may be mediated by alpha-1 adrenergic receptors on smooth muscle.
T139 What is the most common type of prostate cancer and how prevalent is it?
Most prostate cancers (95%) are adenocarcinomas.
Prostate adenocarcinoma is the most common form of cancer in men, usually seen in older age (99% with clinical disease are age 50+).
It is the 2nd most common cancer-related death in men.
What role do androgens play in the development of prostate adenocarcinoma?
Androgens are crucial as cancer does not develop in males castrated before puberty.
Tumor resistance to anti-androgen therapy often involves mutations that allow androgen receptors to activate target genes without hormones.
How does heredity influence the risk of prostate cancer?
Increased risk among first-degree relatives.
Higher prevalence in African origin, lower in Asian origin.
Mutations in BRCA1, BRCA2, and HOXB13 genes increase risk.
People inherit an increased risk of cancer, not the disease itself.
Which genetic variations are associated with an increased risk of prostate cancer?
Variant near MYC oncogene on chromosome 8 (African males).
Susceptibility locus on chromosome 1q24-q25 (American men).
Gene rearrangements creating fusion genes with ETS family transcription factors.
Mutations activating PI3K/AKT pathway, inactivating PTEN tumor suppressor gene.
Loss of PTEN, TMPRSS2–ERG chromosome fusion, p53 mutations, overexpression of MYC.
How do environmental factors influence the risk of prostate cancer?
Aging and diet contribute to the risk.
Incidence increases in Japanese immigrants to the USA.
Where does prostate adenocarcinoma usually arise and how is it detected?
Usually arises from the peripheral zone (posterior and lateral).
Most carcinomas detected clinically are not visible grossly.
Advanced lesions appear as ill-defined, firm, gray-white masses infiltrating adjacent gland.
What are the histological characteristics of prostate adenocarcinoma?
Moderately differentiated adenocarcinoma producing well-defined glands.
Glands are smaller than benign glands in a back-to-back pattern with scant to moderate stroma.
Complete absence of basal cell layer around malignant glands.
Tumor cells have darker stained cytoplasm, enlarged nuclei, and prominent nucleoli.
Presence of perineural invasion and abundant intraluminal mucin.
How are peripheral gland prostate cancers detected during a physical examination?
May be palpable in rectal examination as irregular hard nodules.
Can only identify tumors that are big enough to feel.
How are most localized prostate cancers discovered?
Clinically silent and don’t press the urethra.
Discovered by routine serum PSA level checks in older males.
PSA levels rise with prostate cancer and serve as a warning that the prostate gland has gone awry.
What is PSA, and how is it used in prostate cancer?
PSA (prostate-specific antigen) is a protein produced by cells of the prostate gland.
Levels of circulating PSA rise with prostate cancer.
A serum level of 4 ng/mL is the cutoff between normal and abnormal.
PSA is used for follow-up treatment and recurrence detection, not diagnosis.
What is the Gleason grading system in prostate cancer?
Based on architectural growth pattern rather than nuclear features.
Identifies five grading patterns from 1 to 5, with predominant and second-most predominant grades yielding a combined score.
Grade 1: Most well-differentiated tumors.
Grade 5: No glandular differentiation, higher score suggests worse prognosis.
Describe Gleason grade 1 and 2 prostate tumors.
Gleason grade 1: Single and separate rather uniform acini with little intervening stroma, well demarcated.
Gleason grade 2: Moderate amounts of intervening stroma, not sharply delineated, tumor acini lined by a single layer of columnar epithelial cells, no basal cells.
Describe Gleason grade 3 and 4 prostate tumors.
Gleason grade 3: Small, separate, round to irregular glands with moderate to abundant intervening stroma, most common pattern.
Gleason grade 4: Tumor glands show gland fusion, small to indistinct lumens, complex, cribriform and confluent glands almost without any intervening stroma.
Describe Gleason grade 5 prostate tumors.
Solid tumor with little gland formation.
Poorly differentiated single cells in an infiltrative or sheet-like pattern.
What symptoms might indicate prostate cancer metastasis?
May present with lower back pain secondary to bone metastases.
Spread to lumbar spine or pelvis is common, causing osteoblastic (bone-producing) lesions.
T140 What is cervicitis and its common symptoms?
Inflammation of the cervix, often associated with a purulent vaginal discharge.
Common pathogens include Chlamydia trachomatis (most common), Neisseria gonorrhoeae, Trichomonas vaginalis, Candida albicans, HSV-2, and certain types of HPV.
What are the macroscopic features of cervicitis?
Hyperemia (increased blood flow).
Leukorrhea: flow of a whitish, yellowish, or greenish vaginal discharge.
What are the microscopic features of chronic cervicitis?
Chronic inflammation with regeneration of epithelium.
Epithelium may show hyperplasia and squamous metaplasia of the columnar epithelium.
What is the difference between acute and chronic cervicitis microscopically?
Acute cervicitis: Rare, typically postpartum, and caused by staphylococci or streptococci.
Chronic cervicitis: More common, showing inflammation, regeneration, hyperplasia, and squamous metaplasia.
What are noninfectious causes of cervicitis?
Local trauma (e.g., cervical irritation caused by tampons).
Chemical irritation or inflammation (e.g., Behçet syndrome).
What are common pathogens associated with cervicitis?
Chlamydia trachomatis (most common).
Neisseria gonorrhoeae.
Trichomonas vaginalis.
Candida albicans.
HSV-2.Certain types of HPV.
What are the most common types of cervical neoplasia and their causes?
Most tumors are of epithelial origin, caused by oncogenic strains of HPV.
Common types: Squamous cell carcinoma (SCC) and adenocarcinoma.
Key risk factor: High-risk HPV infection (types 16, 18).
Secondary risk factors: Smoking and immunodeficiency.
What are the primary anatomical regions of the cervix relevant to neoplasia?
Exocervix: Visible on vaginal exam, lined by nonkeratinizing squamous epithelium.
Endocervix: Lined by a single layer of columnar cells.
Transformation zone: Transition point between the exocervix and endocervix.
Describe the pathogenesis of cervical neoplasia.
High-risk HPV infection is the primary cause.
Persistent HPV infection can lead to cervical intraepithelial neoplasia (CIN), a precursor to invasive cervical carcinoma.
HPV oncoproteins E6 and E7 inactivate tumor suppressors p53 and Rb.
Somatic mutations in the LKB1 gene (20%).
What are the main HPV types associated with high-risk and low-risk infections?
High-risk HPV: Types 16 and 18.
Low-risk HPV: Types 6 and 11, which typically lead to condyloma (benign neoplastic lesion).
What is the progression of cervical intraepithelial neoplasia (CIN)?
CIN can progress from dysplasia to carcinoma in situ and eventually to invasive carcinoma if left untreated.
How does HPV contribute to the development of cervical neoplasia?
HPV infects the lower genital tract, particularly the transformation zone of the cervix.
HPV E6 protein binds and inactivates p53.
HPV E7 protein binds and inactivates Rb.
These actions lead to uncontrolled cell growth and progression to neoplasia.
What is the peak age incidence of Cervical Intraepithelial Neoplasia (CIN) and carcinoma?
Peak age incidence of CIN: ~30 years.
Peak age incidence of carcinoma: ~45 years.
What characterizes Cervical Intraepithelial Neoplasia (CIN)?
Koilocytotic change.
Loss of cellular maturation.
Nuclear atypia (cell pleomorphism).
Parakeratosis/dyskeratosis.
Increased mitotic activity within the cervical epithelium.
Describe the different grades of CIN based on the extent of epithelial involvement.
CIN I: Involves < 1/3 of the thickness of the epithelium.
CIN II: Involves < 2/3 of the thickness of the epithelium.
CIN III: Involves slightly less than the entire thickness of the epithelium.
Carcinoma in situ (CIS): Involves the entire thickness of the epithelium
What is the difference between dysplasia and carcinoma in situ in the context of CIN?
Dysplasia is reversible.Carcinoma in situ is not reversible.
The higher the grade of dysplasia, the more likely it is to progress to carcinoma and the less likely it is to regress to normal.
What are LSIL and HSIL, and how do they relate to CIN?
LSIL (Low-grade squamous intraepithelial lesion): Includes HPV, mild dysplasia, CIN 1.
HSIL (High-grade squamous intraepithelial lesion): Includes moderate and severe dysplasia, carcinoma in situ, CIN 2, and CIN 3.
What are the most common types of invasive carcinoma of the cervix?
Squamous cell carcinomas (75%).
Adenocarcinomas and mixed adenosquamous carcinomas (20%).
Small cell neuroendocrine carcinomas (less than 5%).
Where do invasive carcinomas of the cervix typically develop?
In the transformation zone of the cervix.
They can range from microscopic foci of stromal invasion to grossly conspicuous exophytic tumors.
What is a “barrel cervix”?
A condition where tumors encircle the cervix and penetrate into the underlying stroma, producing a barrel-like appearance of the cervix, often identified by direct palpation.
What is a common cause of death in advanced cervical carcinoma?
Hydronephrosis with postrenal failure due to the tumor invading through the anterior uterine wall into the bladder and blocking the ureters.
How effective is the Pap smear as a screening tool for cervical carcinoma?
Very effective.
Cells are scraped from the transformation zone using a brush and analyzed under a microscope to detect neoplastic changes.
T142 + 143 What are the two components of the body of the uterus?
Endometrial mucosa.
Underlying smooth muscle myometrium.
What is endometritis?
Inflammation of the endometrium, classified as acute or chronic based on the type of inflammatory infiltrate present.
What typically causes acute endometritis?
Bacterial infection (e.g., N. gonorrhoeae) of the endometrium.
Usually due to retained products of conception acting as a nidus for infection.
What are the clinical features of acute endometritis?
Fever.
Abnormal uterine bleeding.
Pelvic pain.
What characterizes chronic endometritis?
Presence of plasma cells (necessary for diagnosis).
Lymphocytes are normally found in the endometrium but plasma cells indicate chronic inflammation.
What are some causes of chronic endometritis?
Retained products of conception or intrauterine devices.
Chronic pelvic inflammatory disease (e.g., Chlamydia).
Tuberculosis (granulomatous endometritis).
What are the clinical features of chronic endometritis?
Abnormal uterine bleeding.
Abdominal pain.
Infertility.
What is endometriosis?
Endometriosis is the abnormal presence of endometrial glands and stroma outside the endomyometrium.
What percentage of women in their reproductive years are affected by endometriosis, and what is its association with infertility?
Affects 10% of women in their reproductive years.
Found in nearly half of women with infertility.
What are the common locations of endometriosis?
Ovaries (most common).
Pouch of Douglas (pain in defecation/rectovaginal septum).
Uterine ligaments (pelvic pain/peritoneum).
Fallopian tubes (may cause scarring and infertility, provide area for ectopic pregnancy implantation).
Rarely in the lung/skeletal muscle.
What are the three hypotheses explaining the origin of endometriotic lesions?
Regurgitation theory: Menstrual backflow through the fallopian tubes leads to implantation of endometrial tissue.
Metaplastic theory: Endometrial dysplastic differentiation of coelomic epithelium (of Mullerian duct).
Vascular or lymphatic dissemination theory.
Does endometriotic tissue contain functioning endometrium?
Yes, endometriotic tissue almost always contains functioning endometrium.
What are the key inflammatory and hormonal changes observed in endometriosis?
Increased levels of inflammatory mediators, particularly prostaglandin E2.
Increased estrogen production due to high aromatase activity of stromal cells.
These changes enhance the survival and persistence of the endometriotic tissue within a foreign location.
How does endometriosis differ from adenomyosis in terms of endometrial tissue?
Endometriosis almost always contains functioning endometrium, which undergoes cyclic bleeding, while adenomyosis does not typically contain functioning endometrium.
What gross appearance do endometriotic implants usually have?
They appear as red-brown nodules or implants lying on or just under the affected serosal surface.
What characteristic appearance do endometriotic lesions have when the ovaries are involved?
The lesions may form large, blood-filled cysts that turn brown, known as “chocolate cysts.”
What are the three histological features required for the diagnosis of endometriosis?
The presence of two out of the following three features: endometrial glands, endometrial stroma, and hemosiderin pigment.
What are the clinical features of endometriosis?
Dysmenorrhea (painful menstruation).
Pelvic pain resulting from intrapelvic bleeding and periuterine adhesions.
Specific signs depend on the location of the endometriotic implants.
What causes the pelvic pain associated with endometriosis?
Pelvic pain in endometriosis is caused by intrapelvic bleeding and the formation of periuterine adhesions.
What is adenomyosis?
Adenomyosis is the presence of endometrial tissue within the myometrium.
How does the endometrial tissue in adenomyosis differ from that in endometriosis?
The endometrial tissue in adenomyosis is nonfunctioning and derives from the stratum basalis, hence it does not undergo cyclic bleeding, unlike the functioning endometrial tissue in endometriosis.
What effect does adenomyosis have on the myometrium?
Adenomyosis induces reactive hypertrophy of the myometrium, resulting in an enlarged, globular uterus with a thickened uterine wall.
Why does adenomyosis not cause cyclic bleeding?
The glands in adenomyosis derive from the stratum basalis of the endometrium, which does not undergo cyclic bleeding.
What is dysfunctional uterine bleeding?
Dysfunctional uterine bleeding is abnormal bleeding from the uterus in the absence of a primary organic uterine lesion.
What are the general forms of abnormal bleeding associated with dysfunctional uterine bleeding?
Menorrhagia: Intense or prolonged bleeding at the time of the period.
Metrorrhagia: Irregular bleeding between periods.
Postmenopausal bleeding.
What are common causes of dysfunctional uterine bleeding?
Common causes include endometrial polyps, leiomyomas, endometrial hyperplasia, endometrial carcinoma, and endometritis.
How does the probable primary cause of uterine bleeding vary?
The probable primary cause of uterine bleeding depends somewhat on the age of the patient.
What are the four groups of causes for abnormal uterine bleeding?
Failure of ovulation
Inadequate luteal phase
Contraceptive-induced bleeding
Endomyometrial disorders
What is the dominant cause of abnormal bleeding at both ends of reproductive life?
Failure of ovulation, which results in an excess of estrogen relative to progesterone.
Inflammatory carcinoma
Tubular carcinomas
