MED 482 Diseases of female reproductive system Lecture 1, Exams of Nursing

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Diseases of female reproductive system: Lecture 1 Viral vaginal infections: Genital herpes simplex virus: - HSV 2 infections - Painful red lesions - Virus can travel to the lumbosacral ganglion  latent infection - Dx: multinucleated giant cells (Tzanck smear) - Rx: acyclovir (block DNA synthesis) Molluscum contagiosum: - Poxvirus infection of the skin and mucous membranes - Affect  1) small children 2) adults via sexual transmission - Gross: multiple little papules on the skin, dome shaped papules with dimpled center - In Adults: o Biopsy and histology: epithelial cells overloaded w/ virus (molluscum bodies) - Tx: local destruction Vaginitis: - Inflammation of the vagina - Bacterial, candida, trichomonas vaginalis - Bacterial  Gardnerella vaginalis MCC, risk factor = pregnancy, IUD, douching - Candida  MCC in diabetics and immunocompromised, seen in chronic Ab use - Trichomonas vaginalis  sexual transmission, protozoa Gardnerella vaginalis: - Malodorous fishy smell discharge from vagina o After adding KOH - Pap smear  clue cells = epithelial cells with shaggy coat/granulation of bacteria - Dangerous in pregnant patients = premature labor - Rx: metronidazole Candidiasis: - Erythema in labial areas, very rare to give white film - Risk factors  diabetes and antibiotics - Pap smear  treat with KOH to melt human cells and leave fungal cells o Yeast and true hyphae/pseudohyphae Trichomonas vaginalis: - Amoeba - C/F: strawberry colored mucosa of cervix on colonoscopy - Risk  sexual transmission, males are asymptomatic - Dx: trophozoites with tail (motile flagellates) - Tx: metronidazole Chlamydia trachomatis: - Causes inflammation of the cervix, uterus, fallopian tubes, and lymph nodes o Follicular cervicitis and lymphogranuloma venerum + conjunctivitis in babies - Inguinal lymph node enlargement - Biopsy: necrotizing granuloma + neutrophils + macrophages with inclusion bodies - Can cause  infertility - Tx: azithromycin, doxycycline + for babies with trachoma give erythromycin Pelvic inflammatory disease (PID): - Combination of inflammation of vagina, cervix, uterus, and fallopian tube (entire FRT) o MC problem is in the fallopian tubes and ovaries - C/F: pelvic pain, adnexal tenderness, fever, vaginal discharge - Causes  Neisseria and Chlamydia (staph aureus in patients who use tampon – sepsis) - Acute suppurative salpingitis: o Inflammation of the fallopian tube (neutrophils, plasma cells, lymphocytes) - Consequences of PID: o Infertility o Ectopic pregnancy o Sepsis Diseases of vulva: - External genitalia Bartholinitis: - Obstruction of ducts of Bartholin glands  can cause abscess or cysts - Cysts filled with transudate, abscess filled with exudate - Tx: surgical removal Caruncle: - Fibroepithelial polyps of the urethra - Result of chronic inflammation  granulation tissue that looks like a polyp o Excessive proliferation of CT of urethra Vulvar vestibulitis associated with vulvodynia: - Vulvodynia  burning discomfort, itching, throbbing, and tenderness in vulva Leukoplakia: - White plaques in the walls of vulva - Can be caused by variety of diseases: o Inflammatory dermatitis, psoriasis o Invasive carcinoma o Lichen sclerosis and Lichen simplex LSA and LS can cause leukoplakia Lichen sclerosis (LSA)  autoimmune atrophic skin LSA = ATROPHY - Thinning of epidermis, superficial keratosis - Increased chance of developing squamous cell carcinoma - Whitish plaques + rough skin = discomfort and painful - Biopsy: mucosal atrophy + fibrosis + inflammation Lichen simplex  autoimmune hypertrophic skin  squamous cell hyperplasia - Rough skin and hyperplastic epidermis NOT atrophic Condyloma acuminatum: - Sexually transmitted HPV 6 and 11 (not precancerous) - Spiked shape of condyloma unlike flat condyloma of syphilis - Morphology  koilocytic atypia o epithelial cells look round, nucleus shrink, clear cytoplasm Vulvar intraepithelial neoplasia (VIN): - Risk factors : multiple partners, young age of intercourse, persistent infection with HPV - HPV infects immature basal cells in squamous epithelium at squamo-columnar junction - HPV inactivates tumor suppressor genes in epithelial cells Viral E6 inhibits p53 Viral E7 inhibits Rb - Classification: LSIL (low grade = dysplasia) and HSIL (high grade = carcinoma in situ) o Koilocytosis = sign of HPV infection - LSIL (if not treated)  HSIL  invasive cervical carcinoma - LSIL to HSIL may take from months to more than a decade Invasive cervical carcinoma: - Microinvasion of malignant cells into the BM of cervix - 80%  squamous cell carcinoma (MC) o Keratin pearls, cytokeratin staining, intracellular bridges - Peak age of development = 45 years - C/F: asymptomatic, malodorous discharge, pelvic pain, postcoital bleeding - Complications: o Invade rectum, bladder, ureters (hydronephrosis and renal failure) - Treatment: chemotherapy - Prevention: pap smear, vaccinations Pap smear screening: - 21 years of age or 3 years of onset then annual basis - HPV DNA testing  if positive, woman has to have repeatable DNA test every 6 – 12m - If Pap test abnormal o Colposcopic examination of cervix and vagina o Tissue biopsy  Dx HSIL and LSIL o HSIL  excision o Abnormal = increased N:C ratio Diseases of uterus: Endometrium: Stages of menstrual cycle  four phases - Follicular (proliferative) – mid cycle – luteal (secretory) – menses - Menstrual cycle = 28 days - Variability in length of cycle determined by follicular phase - Follicular/proliferative phase = increased estrogen o Estrogen from corpus luteum - Luteal/secretory phase = increased progesterone  stimulate secretory phase o Progesterone from corpus luteum - LH spike at the time of ovulation - GnRH  FSH, LH  estrogen, progesterone Proliferative phase: - Many glands rapidly growing with increase mitosis Secretory phase: - Mucus releases into gland - Corpus luteum  corpus albicans, progesterone decreased  cells apoptosis Dysfunctional uterine bleeding: Functional disturbances in endocrine system is MCC - Anovulatory cycle, inadequate luteal phase, OCPs, menopause, post-menopause - Anovulatory cycle: o Follicle not ruptured  oocyte remains inside  granulosa cells continue to produce estrogen  stimulate proliferation of endometrium o Rupture of follicle needs LH spike o Causes: hormonal imbalance, endocrine disease (thyroid, adrenal, pituitary), polycystic ovary syndrome, obesity (excess estrogen), severe malnutrition Amenorrhea/Anovulation: - Irregular cycles of bleeding - Primary  absent menses age 16 - Secondary  absences of menses for 3 months in woman with previous normal cycle - Causes: o Hypothalamic dysfunction  stress, anorexia , obesity o Pituitary infarcts o Ovarian diseases o Asherman’s syndrome  intrauterine scarring following abortion - Decrease adipose  decreased leptin  low GnRH  low FSH, LH  low estrogen Inadequate luteal phase: - Normally corpus luteum turns to corpus albicans - In inadequate luteal phase  low progesterone and frequently bleeding o Short secretory phase - Complications with fertility Menopause and post menopause changes: Menopause: - Anovulatory cycles  uninterrupted estrogen  hyperplasia and cysts in endometrium - Endometrium sloughs off and cause bleeding  iron deficiency anemia Post menopause: - Ovarian and endometrial atrophy - Cystic atrophy may damage and cause bleeding Acute endometritis: - Causes: o Bacterial: group A hemolytic streptococci, staphylococci  sepsis o Retained products of conception after delivery or abortion - C/F: pain, cramping, vaginal discharge, fever, constipation - Histology: neutrophilic infiltrate Chronic endometritis: - Causes: o Sexually transmitted pathogens: chlamydia, Neisseria o Intra uterine devices (IUD) o Mycobacteria - Biopsy: plasma cells in the endometrium is diagnostic Endometriosis: - Normal endometrial glands outside the myometrium/uterus - Pathogenesis theories: o Regurgitation theory  retrograde flow of endometrial cells to peritoneal cavity o Vascular/lymphatic dissemination  similar to a cancer o Metaplastic theory  endometrial tissue planted during embryogenesis - Endometrial tissue in ovaries = cysts “ chocolate cysts ” / endometriomas - C/F: pain caused by nodules releasing PG, periodic bleeding, infertility - Dx: 3 D’s  dysmenorrhea , dyspareunia , dyschezia - Treatment: aromatase inhibitors = block menstrual cycles because decreased estrogen Adenomyosis: - “endometriosis interna” - Endometrial glands grow INTO the myometrium - C/F: painful prolonged periods, infertility - Inflammation and increased contractility of uterus  large size of uterus - Differentiate from pregnancy by checking beta-HCG Endometrial Polyps: - 0.5 to 3 cm polyps - Histology: endometrial glands resembling stratum basalis - Predisposing factor  estrogen (administer of anti-estrogenic drug Tamoxifen) o Stimulate proliferation of endometrium Endometrial hyperplasia: - Endometrial glands excessively proliferate - Disappearance of stroma - Cause: high level of estrogen  proliferation of endometrium o Anovulatory cycles o Ovarian tumors o Mutation in gene PTEN  cells proliferate actively because no tumor suppression - Endometrial hyperplasia may be transformed into endometrial carcinoma - Morphology: o Endometrial hyperplasia with simple and complex atypia and without atypia Carcinoma of endometrium: - Between 55 – 65 years of age - MC invasive cancer of female genital tract in US - Adenocarcinoma type I o 80% of all patients o As a result of endometrial hyperplasia  Obesity, diabetes, HTN, infertility, unopposed estrogen stimulation o Pathogenesis: o Serous tumor , mucinous tumor are MC  epithelial tumors most likely bilateral o Classification:  Benign , borderline , malignant  Malignant – stromal invasion and atypia - C/F: o Very little symptoms, but metastasis o Vaginal bleedings Epithelial tumors : Markers = CA-125 + osteopontin - Most likely bilateral, prevent with OCP’s - Coelomic epithelium – give rise to many subtypes of epithelium o Tubal serous epithelium (fallopian tube)  serous tumor o Endometrial epithelium  endometrioid tumor o Mucinous (cervical) epithelium  mucinous tumor o Transitional epithelium  Brenner tumor o Kidney like epithelium  clear cell tumor 1. Serous tumor: CA-125 - Cystic tumor with clear serous fluid - Polyp growth inside the tumor - Can be benign (serous cystadenoma), borderline, malignant - Serous adenocarcinoma  most likely bilateral - Pathogenesis: Nulliparity, family history, gene mutations (BRCA1) - Morphology: Cysts filled with clear/yellow fluid - Histology: o Benign serous cystadenoma  Psammoma bodies (concentric calcification) o Serous adenocarcinoma  infiltration of underlying stroma, marked nuclear atypia, pleomorphism, atypical mitotic figures, multinucleated 2. Mucinous tumor: - Mutation of KRAS - Morphology: o Large cystic masses with many little cysts (sponge like) o Sticky clear mucinous (gelatinous) fluid rich in glycoproteins o Benign, borderline, malignant - Biopsy: o Many clear cells filled with mucin o Resemble cervical epithelium - May spread beyond the ovary  poor prognosis o Pseudomyxoma peritonei mucin in the peritoneal cavity (mucinous ascites) 3. Endometrioid tumor: - Resemble endometrial glands - Pathogenesis: Mutation in PTEN  overly active cell proliferation - Morphology: Bloody tissue in autopsy - Histology: o Multiple glands (late stage endometrium/ secretory phase) 4. Clear cell tumor: - Benign, borderline, malignant (clear cell carcinoma) - Large epithelial cells with clear cytoplasm - Resemble clear cell carcinoma of the endometrium (gestational endometrium) 5. Brenner Tumor: - Mostly benign, rarely malignant  transitional cell tumor (resemble urinary system) - Histology: o Nests of transitional type epithelial cells resembling those lining the urinary bladder  mix of cells - No cysts in the tumor, solid white yellow color tumor C/F of all epithelial ovary tumors  ascites, urinary frequency, GI complaints, metastasis Germ cell tumors: 1. Teratoma: Benign/Mature  - Cysts growing on the ovary, inside is well differentiated bone, skin, hair tissue etc. - Karyotype of benign teratoma: 46,XX - 2 subtypes: solid + cystic (dermoid cysts) o Dermoid cysts  teratoma that contains skin derivatives (sebaceous gland, hair, sweat glands, etc.) o Monodermal teratoma  one well developed organ in the cysts (ex: thyroid)  Struma ovarii  ovarian tumor producing T3 and T4 (hyperthyroidism) 2. Dysgerminoma: - Ovarian counterpart of seminoma in testes - Histology: identical to seminoma o Salt and pepper pattern  dark round lymphocytes spread between clear cells - Markers: OCT3/4, Nanog, c-KIT - C/F: pseudo-hermaphroditism is risk factor 3. Yolk sac tumor: (endodermal sinus tumor) - Derived from embryonal yolk sac structure - Schiller Duval bodies (pseudo rosettes) - Rich in alpha fetoprotein and alpha 1 antitrypsin - Risk factor  age (young adult females) 4. Embryonal carcinoma: - Tumor of young girls (< 14 years) - Necrosis - Beta HCG = marker - Histology  primitive glandular structures Stromal tumors: - Tumors from Leydig, granulosa, and theca cells o Graafian follicle lined with granulosa cells which secrete ESTROGEN o Outside of follicle are theca cells secrete ESTROGEN o In stroma of ovary there are Leydig cells secrete ANDROGEN 1. Granulosa – Theca cell tumor: - Histology: immature follicles - Normally secrete estrogens - Marker  inhibin - Side effect on endometrium  endometrial hyperplasia and carcinoma - Ex: 65 year old women has heavy uterine bleeding, endometrial biopsy = hyperplasia 2. Fibroma/thecoma/fibrothecoma: - Tumor derived from theca cells (elongated fibroblast looking cells) - Produce estrogen  endometrial hyperplasia and bleeding - Meigs syndrome : o Ovarian tumor released factors that cause accumulation of fluid in thoracic and abdominal cavity o Transudate in thoracic cavity  hydrothorax (very specific for fibroma) Metastasis  Kruckenburg tumor: MC metastasis to ovary = diffuse type signet ring cell gastric carcinoma Pseudomyxoma peritonei  mucin in the peritoneum Disorders of pregnancy: - Early (< 20 weeks) and Late (> 20 weeks) pregnancy diseases 1. Spontaneous abortion: - Loss of pregnancy before 20 weeks (stillbirth is after 20 weeks) - 50% before week 12 - 20% of pregnancies end in spontaneous abortion o MCC  problem with fetus (chromosomal anomalies + severe mutations)  Aneuploidy, polyploidy, translocations etc. - First semester maternal causes: o Short luteal phase in mother  corpus luteum degrade quickly o Poorly controlled diabetes + endocrine problems o Physical defects in uterus  leiomyoma - Second semester: o Fetal anatomical abnormalities o Maternal causes  toxoplasma, mycoplasma, listeria, antiphospholipid Ab syndrome (blood coagulation in placenta), coagulopathies, HTN - Third semester: o Placental insufficiency 2. Ectopic pregnancy: - Implantation of fetus in any site other than intrauterine location