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50 Cards in this Set

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What are the causes of abnormal uterine bleeding in different age groups?
PRE-PUBERTY: precocious puberty
ADOLESCENT: anovulatory cycle, pregnancy
REPRODUCTIVE/PERIMENOPAUSAL: pregnancy, anovulatory cycles, polyps, endometriosis, hyperplasia, carcinoma
POST-MENOPAUSAL: polyps, hyperplasia, carcinoma, atrophy
What is endometrial hyperplasia?
-abnormal proliferation usually caused by prolonged periods of estrogen stimulation; as hyperplasia becomes architecturally and cytologically atypical it can become independent of hormones and autonomously grow
-can be precursor of carcinoma; see increased crowding of glands and abnl contour
-classification: SIMPLE- slight increase in glands to stroma ratio, no cytologic atypia (simple atypical is same with cytologic atypia), minimal crowding, architectural budding and branching; COMPLEX- marked increase in gland to stroma ratio with no cytologic atypia (complex atypia is same plus cyto atypia)
-cytologic atypia has more of a chance to progress to carcinoma than complex vs. simple
What types of endometrial carcinoma are there?
-endometriod (endometrium) and serous (fallopian tube) are the most common
-clear cell (endometrium in pregnancy), mucinous (cervical gland), adenosquamous (endometrium) are less common
What are the two main biologic endometrial carcinomas?
-Endometrioid ED : "type 1 tumors" are estrogen related, low grade, pre/peri-menopausal, and are preceeded by endometrial hyperplasia
-Non-Endometrioid: "type 2 tumors" are unrelated to estrogen, high grade and aggressive, happen in older women and have an atrophic background
Endometrioid carcinoma
-Hereditary non-polyposis coli syndrome: associated with mutation in DNA mismatch repair genes leading to genetic instability, endometrioid carcinoma is second most common tumor in this syndrome
-most have a loos of DNA mismatch repair genes seen by immunohistochemistry
-Cowden Syndrome: autosomal dominant multiple hamartoma syndrome; increased risk of breast, thyroid, and endometrial carcinoma; germline PTEN gene mutation (sporadic carcinomas may also have loss of PTEN)
-PTEN: expressed in normal proliferative endometrium, expressed in secretory phase, combination of estrogen stimulation and abnl DNA repair sets up an uncontrolled growth and mutator phenotype
Non-endometrioid Carcinomas (Type II)
-frequently associated with atrophic endometrium not hyperplasia
-no association with DNA mismatch repair, microsatallite instability, or PTEN abnormalities
-nearly uniform mutations in p53 (endometriod rarely has p53 mutation)
The Cervix
-normal: ectocervix (stratified squamous epithelium, gylcogenated under influence of estrogen, shows a "basketweave" appearance) endocervix (simple columnar mucinous epithelium, glands are deep invaginations and not true glands
-squamous metaplasia: sequence - reseve cell hyperplasia (basally located) to immature squamous metaplasia (multiple layers of cuboidal reseve cells) to mature squamous metaplasia ( flattening and keritinization of surface cells, "epidermidization")
What is the adenexa? And what are the functions?
-ovaries and fallopian tubes
-ovaries are 3-6grams normally; localized lateral to the uterus and medial to the illiac vessels and pelvic wall; stablized in the pelvis by ligaments (uteroovarian ligament, infundibulopelvic ligament)
-ovaries: have 1-2million follicles at birth, 8000 develop in female lifetime, 300 are released, and cyclically produces estrogen and progesterone from menarche to menopause
What are simple follicular cysts?
-disturbance in follicular function/temporary variation in normal physiologic process; thin walled, smooth and translucent; filled with watery, clear to straw colored fluid
-presentation: majority are asymptomatic (discovered through routine exam), occasional abnol menstrual activity, pain or pressure in pelvis
-treatment: observation (can regress or "silently" rupture), OCPs to block gonadotrophin actions on the cyst, needle drainage, laparoscopy or laparotomy
What is a hemorrhagic cyst (corpus luteum)?
-develops from a mature graffian follicle, spontaneous bleeding following ovulation fills the follicle (can cause rupture); can be associated with normal endocrine function or prolonged secretion of progesterone with delay in menses
-presentation: asymptomatic; cull, unilateral pelvic pain; rarely can cause massive intraperitoneal hemorrhage
-treatment: observation, OCPs, laparoscopy (cystectomy) or laparotomy (cystectomy or oopherectomy)
What is an endometrioma?
-endometriosis cyst of the ovary; functioning endometrial tissue outside of the uterine cavity; benign and progressive dz with a definitive diagnosis by biopsy
-presentation: chronic pelvic pain (can be localized); acute pelvic pain/pressure; infertility; or incidental finding
-can rupture or cause torsion if untreated
-treatment: stopping ovarian function (natural or induced menopause, OCPs or depo-provera), endometrioma (cystectomy or oopherectomy)
What is a paratubal cyst?
-thin walled, smooth cyst adjacent to the fallopian tube/ovary, can be mesonephric, mesothelial, or paramesonephric duct origing
-presentation: asymptomatic; dull pain; torsion
-treatment: observation; surgical treatment with drainage or excision
What kinds of ovarian tumors are there?
EPITHELIAL: serous cystadenoma, serous cystadenocarcinoma, mucinous cystadenoma/adenocarcinoma, endometrioid carcinoma, benign brenner tumor
GERM CELL: mature teratoma (dermoid), immature teratoma (malignant), dysgerminoma, epidermal sinus tumor, choriocarcinoma
SEX CORD STROMAL: thecoma, sertoli-leydig cell tumor, granulosa cell tumor
Epithelial Tumors of the Ovary
-most frequent ovarian neoplasm (2/3), arise from coelomic epithelium and many are bilateral (esp. if malignant)
-presentation: usually detected as a mass on pelvic exam, swollen abdomen with vague discomfort, diagnosis frequently made after spread
-treatment: staging surgery (pelvic washings, ascites, total hysterectomy, bilateral salpino-oophorectomy, omentectomy, paraaortic and pelvic lymph node sampling); chemo and intraperitoneal therapy
What is the staging/grading and survival of epithelial ovarian tumors?
-staging: I (limited to ovaries) II (ovaries plus) III (limited to pelvis/small bowel/ommentum/liver) IV (distant mets)
-grading: judge how closely lesion looks like the cell of origin, does not have prognostic value for clear cell carcinoma
-survival: I-80%, II-60%, III-23%, IV-14%
Germ Cell Tumors
-account for 20-25% of tumors and 2-3% are malignant (higher chance in women < 21), usually unilateral
-TERATOMA: 33% of benign ovarian neoplasms, mainly a cystic structure containing elements from 3 germ cell layers (mature/bening (dermoid) malignant ("immature")); arise from single germ cell after first meiotic division (totipotent stem cell, 46XX, differs from host); presentation- asymptomatic, pelvic pain/pressure, torsion, rupture, hemorrhage; treatment - laparoscopy, laparotomy
-DYSGERMINOMA: most frequent malignant germ cell, primitive germ cells with stroma infiltrated by lymphocytes; occurs primarily in women <30, prognosis related to size, encapsulation, metastasis and lack of ascities, usually present at stage IA with a >90% survival
Granulosa Cell Tumor
-varying proportion of theca cells and/or fibroblasts; surrounded by eosinophillic bodies; function tumors are estrogenic and 5% occur before puberty
-presentation: prepubertal (precocious puberty), postmenopausal (bleeding, endometrial carcinoma (5%)), reproductive (abnl bleeding), tumor rupture
-treatment: unliateral salpingo-oopherectomy, chemotherapy, radiation, follow inhibin levels
Ovarian Cancer
-leading cause of death from gynecologic malignancies in US
-mean age of occurance is 60; associated with nulliparity, history of colon or breast cancer, first degree relative affected, prolonged use of fertility drugs
Spontaneous Abortion
-early fetal loss <20wks or <500 grams, 10-20% of clinically recognized pregnancies, 80% occur <12 weeks
-chromosomal abnormalities >50% and risk increases with age and parity (35yrs- 20%, 40 yrs- 40%, 45- 80%)
-MATERNAL CAUSES: age, infection (herpes, HIV, Parvo, syphillis, group B strep, Mycoplasma, ureaplasma), diabetes (control in the 1st trimester), insufficient progesterone, tobacco, alcohol, caffeine, radiation, NSAIDs, autoimmune abs (lupus anticoag, antiphospholipid abs), inherited thrombophilias (protein C, S, ATIII def., factor V Leiden), incompetent cervix (dilation in 2nd trimester)
-histologically will see hemorrhage into necrotic decidua basalis and placental villi that are edemetous or devoid of blood vessels
-symptoms: vaginal bleeding (50% abort) and cramping
Ectopic Pregnancy
-1/100 pregnancies
-leading causes of maternal mortality: hemorrhage, embolism, HTN disorders (preeclampsia, chronic HTN) and ectopic pregnancy
-locations: fallopian tube (90%), ovary, cervix, cornual/interstitial, and abdominal
-incidence is increasing, conditions associated are: salpingitis- adhesions from surgery, prior ectopic, pelvic infection; tubal sterilization; tumors; DES exposure; and capacity to control pregnancy (elective ab, IUD, IVF, corrective tubal surgery)
-mortality is decreasing
-presentation depends on location of implant, amount and rapidity of bleeding; classic triad - pain (abdominal or shoulder), amenorrhea and vaginal bleeding
-evaluation: history and physical; labs (CBC, quantitation of beta hCG (doubling time 48 hours in most normal pregnancies), progesterone <10ng/ml is very suspicious of abn. pregnancy)
-treatment: surgical (laparoscopy and laparotomy, salpinostomy and salpingectomy) and medical (methotrexate - folic acid antagonist binding to DHreductase; safe and effective, single and multiple dose, lower cost and morbidity, can be used in surgical failure)
-outcomes after ectopic: conception ~55%, repeat ectopic risk is higher
Problems with Placentation
-previa: implants over the cervix and blocks the os, severe antepartum hemorrhage with contractions or cervical dilation, increased risk with previous C-section scar, results in third trimester hemorrhage, premature separation during delivery will lead to hypoxia
-accreta: absence of normal decidual plate with chorionic villi extending into myometrium, 60% are associated with previa, risk factors: abortion, curettage and general scarring; increta (invasion of myometria) and percreta (perforation)
-abruptio: premature ,separation of placenta
-chorionicity is the key
-Dizygotic: fertilization of 2 oocytes (non-identical), all are dichorionic (has it's own amnion, chorion and placenta), 2/3 of twins born; prevalence varies with ethnic group, maternal age, parity and ovulation induction; on ultrasound will see twin peak (lambda sign)
-Monozygotic: splitting of one embryonic mass to form 2 genetically identical fetuses, may share same placenta (monochorionic), amniotic sac (monoamnionic), or organs (conjoined); the later the split the more the complications; 1/3 of twins are monozygotic; prevalence doesn't vary; monochorionic are always monozygotic
-complications - pernatal mortality is five times higher than singletons, higher neonatal death and handicap, preeclampsia is 4x higher, death of one fetus, structural defects, chromosome abnormalities, TTS (twin transfusion syndrome)
-discordant growth: unequal size may be sign of pathology, morbidity and mortality increase with 20% discordancy; di- unequal placenta, diff. genetic growth; mono- more likely, vascular comm. prob.
Twins continued
-management: sonographic monitoring every 3 weeks; BPP doplers weekly, delivery if fetal well being not assured
-death of one fetus: prognosis of other twin depends on gestational age at demise, chorionicity, and length of time between fetal demise and delivery; dichorionic (risk of PTD due to release of cytokines and PGs from the dead placenta, risk of handicap), monochorionic (30% risk of death or neuro handicap due to acute hypotension from hemorrhage into dead placenta)
-chorionicity is main factor for determining risks/pregnancy outcomes
-TTS: no structural malformation just more transfusion to one from abnl placental vascular anastomosis; artery from donor enters placenta and vein returns to other twin(recipient); donor is anemic, IUGR and recipient is polycythemic, high CO failure, and hydrops; w/o treament have 70-80% death; therapy - amnioreduction, interrupt connection
-conjoined twins: types - anterior (thorocopagus, most common), posterior (pyopagus), cephalic (craniopagus) and caudal (ischiopagus); results from twinning initiated after embryonic disc and rudimentary amnionic sac have formed (day 13-15 of life); female to male 3:1; majority are stillborn
-5-10% of pregnancies, pregnancy specific (can occur before, during or after delivery), multisystem disorder, HTN and proteinuria, after 20 weeks gestation
-3rd cause of preg-related deaths; is associated with - placental abruption, acute renal failure, CV and neuro complications, pulmonary edema, DIC and maternal death
-blacks > hispanics > whites
-HTN disorders: chronic HTN(b/f 20 weeks, no/stable proteinuria), Preeclampsia/eclampsia (after 20 weeks, proteinuria), preeclampsia superimposed on chronic HTN (b/f 20 weeks, new/increased proteinuria, HELLP), gestational HTN (after 20 weeks, no proteinuria)
-pathophysiology: abnl placenta--> endothelial injury --> systemic vasospasm, HTN -> endothelial damage, leakage of platelets, tissue hypoxia -> necrosis or hemorrhage in multiple end organs
-HELLP (hemolysis, elevated liver enzymes, low platelets)
-treatment: DELIVERY
-indications for delivery: IUGR, nonreassuring fetal surveilence, maternal distress
-management goals: prevent seizures, control htn, prevent maternal/fetal mortality
-drugs: magnesium sulfate, hydralazine, labetalol, nifedipine
-sflt may be indicated
-early detection, monitoring and treatment are crucial to prevent maternal mortality
Ovulation and Fertilization
OVULATION: day 14 of 28 day cycle, induced by an LH surge, meiosis I complete at ovulation, the most oogonia are present at the second trimester
FERTILIZATION: occurs in fallopian tube w/in 2 days of ovulation, meiosis II complete after fertilization
The Placenta
-the dividing cells differentiate into inner (embryo and amnion) and outer layers (chorion and trophoblastic tissue)
-at 6 days after fertilization the conceptus has infiltrated the endometrium and outer cell mass has differentiated into syncytiotrophoblast and cytotrophoblast
-villi of trophoblast happens by 13 days, placental blood vessels by 17-21 days, embryonic ciculation by 5 weeks and discoid placenta by 13 weeks
-400 to 550 grams (larger in diabetics), inner surface is shiny and covered by the amnion, fetal blood enters villous capillaries through umbilical and placental arteries
Umbilical Cord and Chorionic Villi
UMBILICAL CORD: two arteries and one vein (single artery associated with renal abnormalities), loose matrix (Wharton's jelly), covered by amnion, may have embryonic remnants (allantoic duct, omphalomesenteric duct)
CHORIONIC VILLI: specialized for gas and nutrient exchange, loose CT has fetal capillaries; largest in first trimester and smallest in third, cytotrophoblast more prominent in first trimester and capillaries and syncytiotrophoblasts in the third trimester
What are the errors of implantation?
-positional: placenta previa
-insufficient decidua: placenta accreta, placenta increta, placenta percreta
-components of both: ectopic
What are the causes of first trimester fetal demise?
-1/3 of pregnancies abort in first trimester (2/3 have chrom. abnormalities)
-death of embryo results in "blighted ovum" or empty sac
-causes: mechanical impingement in uterine cavity (leiomyoma, polyp), immune surveillance rejects implant, teratogens
What are the causes of second and third trimester fetal demise?
-cervical incompetance; vascular incompetance (infarction: eclampsia, sickle cell anemia, maternal floor infarct, retroplacental hematoma); infections (ascending: trans-cervical and chorioamnionitis, hematogenous: trans-plancental and villitis)
-premature rupture of membranes is a major risk factor
-there is an early repsonse of maternal neutrophils and membranes and subchorionic plate
-fetal neutrophils migrate through the vessels
-affecting organisms are coliforms and mycoplasma
TOXOPLASMOSIS: protazoan acquired by contact with raw meat or cat poop, 50% risk of fetal infection with maternal infection, causes growth retardation, microcephaly, mental retardation, blindness or deafness
RUBELLA: causes cataracts and hearing defecits, growth retardation and hepatitis; most sensitive period is 3 to 11 weeks; see villitis and edema in the placenta
CYTOMEGALOVIRUS: grossly may be normal, edematous or small for dates; see acute necrotizing villitis and vasculitis with intranuclear inclusions; causes hepatosplenomegally, microcephaly, petechiae, mental retardation, and seizures
SYPHILIS: 50% stillbirth rate; infection can occur in all three trimesters; causes hepatosplenomegally, mucosal fissures, growth retardation, rash and end organ fibrosis
LISTERIA: implicated in spontaneous abortions and neonatal sepsis; spread through contaminated meat; abscesses with purulent villitis
Complete Hydratidiform Mole
-patients come in during 4th or 5th month of pregnancy with absent fetal heart tones and large sizes for dates; swollen, edematous villus structures, circumfrential trophoblastic proliferation and extra-villous trophoblast with no embryonic elements
Partial Hydratidiform Mole and what are moles?
-typically presents as a first trimester miscarriage, there are swollen villi and a fetus may be seen; there is normal sized and large hydropic villi
MOLES ARE.... the father's fault (two sperm (XX or XY) or one sperm (X) with dupication and maternal chromosomes lost with second polar body)
-malignant tumor of cytotrophoblast and syncytiotrophoblast; follows a normal/abnormal pregnancy
-grossly hemorrhagic and necrotic, has both trophoblast types with no villi
-infiltrates myometrium with spread to lungs and brain with elevated hCG levels
-responsive to chemo: advanced stages can respond to single agent MTX; can have subsequent pregnancies
Placental Site Trophoblastic Tumor
-rare tumor of intermediate trophoblastic orgin (cells of implantation area, produce human placental lactogen)
-locally invasive, 5-10% are metastatic, don't respond to chemo, need to be differentiated from normal implantation trophoblast
What is infertility
-one year of unprotected sex without conception (there is a 20-25% chance of conception per cycle)
-advancing age increases the chance of infertility (30-34: 1 in 7, 35-39: 1 in 5, 40-44: 1 in 4)
-peak fertility rates are from 20-24; assisted reproduction decreases with age and miscarriages increase with age
-oocyte factors play more of a role than uterine factors (use of donor eggs for reproduction does not decline with age); aneuploidy of the oocyte increases with age
Evaluation of infertility
-overall causes: male factors 30%, unexplained 25%, tubal/peritoneal disease 20%, ovulation dysfunction 20%
-to evaluate: female-ovulation status, hystersalpingogram, pelvic ultrasound; male: sperm analysis
What are the factors in male infertility?
-low sperm count (not enough getting into cervix)
-immotile/poorly motile sperm (can't reach tube)
-abnormal sperm (can't fertilize)
- should have: >2mL volume, >20million/mL concentration, >50% have forward progression, >30% normal
-to perform intrauterine insemination need to: isolate motile sperm, inseminate through the cervix, need 10 million sperm
-to treat male infertility need to do IVF (insemination of the oocyte directly with sperm)
What are the tubal/peritoneal infertility factors?
-adhesions (fibria can't capture the sperm); blocked tube (sperm can't get to egg); damaged tube (ineffective transport/embryo development)
-determine status of tubes with a hysterosalpingogram
-PID contributes to damage (increases with severity, number and age at time of the infection)
-repair: pros (multiple chances for conception) and cons (tubal patency doesn't garuntee pregnancy, function can be permanately compromised)
How does endometriosis and prior ectopics contribute to infertility?
ENDOMETRIOSIS: causes retrograde menstruation (risk increases with more exposure to menses; lymphatic/hematogenous spread (can implant on all organs); endometrial cells produce an inflammatory response causing scarring (creation of a suboptimal intrauterine environment), also activation of macrophages which may secrete cytokines and kill sperm?
ECTOPIC: increasing incidence due to STD/PID increase, tubal surgery, assisted reproduction and earlier diagnosis
What are the tests for infertility?
-post-coital test (PCT): done midcycle (2-12 hours post coital), mucous is aspirated and examined
-Basal Body Temperature (BBT): temperature increases in response to progesterone and temperature rise occurs after ovulation
-ovulation predictor kits: detects urinary LH, positive test predicts ovulation in next 24-48 hours
-fertility monitors: detect rising estrogen (high fertility) and rising LH (peak fertility)
Polycystic Ovary Disease
-criteria: hyperandrogenism, oligomenorrhea, exclusion of other causes of androgen excess
-need 2 out of 3 criteria: oligo and or anovulation, clinical and/or biochemical signs of hyperandrogenism
-associated with insulin resistance, insulin sensitizers induce ovulation
Ovarian Surface and Stroma
-surface epithelium: has a simple sq. layer, meothelium, invaginates to form cysts, can become metaplastic to form other tissues
-stroma: short spindle cells, hormonally active, cells adjacent to follicle form theca interna and externa of corpus luteum
Germ Cells, Follicles, Corpus Luteum and Corpus Albicans
GERM CELLS: migrate to germinal ridge from yolk sac, 400,000 at birth, locked in meiosis I from birth
FOLLICLES: primordial (single thin layer of granulosa cells), primary (cuboidal layer of endothelial cells), secondary (multiple layers, theca ineterna and externa), tertiary (large, fluid filled spaces)
CORPUS LUTEUM: post-ovulatory follicle, capillary ingrowth into the granulosa layer, see calcifications in pregnancy; granulosa cells (estrogen), theca interna (steriod precursors)
CORPUS ALBICANS: luteum undergoes scarring, retraction of surface pulls mesothelium into the stroma
-composed of glands and stroma
-functionalis shed monthly during reproductive years and regenerated from basalis
-proliferative (glandular lumen communicates with surface, mitotic activity) secretory (3 phases: early- day 16-18 with a single layer of nuclei, mid- more dilated, stroma edematous, late- decidualization)
-menstrual (endometrial stroma falls apart, and begins to desinigrate, fibrin thrombi in arterioles, triggered by progesterones
-myometrium is smooth muscle and the bulk of uterine thickness
-prolonged periods of estrogen with irregular breakdown, common at menarche, low weight, chronic disease, idiopathic
-primary lesion: premature menopause, autoimmune oophoritis, granulosa cell tumor
-hormonal disturbance: thyroid, pituitary, adrenal
-Luteal Phase Defect: early failure of corpus luteum leading to incomplete development of endometrium, period lags behind dates
OCPs and Mechanical causes of infertility
OCPs: contain progesterone, suppress gland proliferation, pseudodecicualization of stroma
MECHANICAL: space occupying (polyp, leiomyoma, IUD, Aschermann's), fallopian tube defects (infection: tuboovarian abscess, chronic salpingitis; endometriosis)
Endometritis (Acute and Chronic)
ACUTE: usually caused by strep, staph, neisseria and chlamydia; associated with pregnancy or abortion, neutrophils
CHRONIC: chylamydia, mycoplasma, retained tissue, IUD, plasma cells
Salpingitis (Acute and Chronic)
ACUTE: inflammatory cells and pus; genococcus, chlamydia, anaerobes, mycoplasma; can cause scarring, hydrosalpinx, tubo-ovarian abscess
CHRONIC: fibrin deposition resulting in adhesions and scarring; cillia and plical motility altered; blind loops can lead to ectopic