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117 Cards in this Set

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What does estrogen do to endometrium?
growth of glands, stroma vessels (follicular phase)
what does progesterone do to endometrium?
differentiation in primed endometrium. See subnucleolar vacuoles
What do contraceptive pills do to endometrium?
scant endometrium with small sparse glands in abundant stroma. Reflect low estrogen with high progesterone
Contrast acute and chronic endometritis
acute = neutrophilic
chronic = plasma cells
What is endometritis assoicated with?
instrumentation, IUD, PID, necrotic tissue in endometrium, outlet obstruction, ascending organisms
Clinical presentation of endometritis?
menometrorrhagia, cervical discharge, uterine tenderness, increased ESR, white count
Describe pathologic features of dysfunctional uterine bleeding
disordered proliferative pattern, irregular gland, fibrin thrombi, focal stromal collapse with pseudovascular pattern
What luteal phase defects can cause dysfunctional uterine bleeding?
inssuficient corpus luteum or irregular shedding with corpus luteum persisting too long
What are pathological features of endometrial polyps?
glands usually weakly proliferative, disordered architecture, cystic dilatation
What is endometrial hyperplasia?
abnormally proliferative endometrium, cx by architectural abnormalities and increased volume
Contrast simple and complex endometrial hyperplasia
simple - total volume increased. Glands haphazardly arranged, commonly cystically dilated with buds and outpouchings.

complex - marked gland complexity and/or crowding. glands have finger in glove appearance.
Prognostic value of cytologic atypia with endometrial hyperplasia
predicts who will progress to adenocarcinoma
Pathogenesis of endometrial hyperplasia
prolonged unopposed estrogen stimulation (inactivation of PTEN gene for example)
Management of endometrial hyperplasia
depends on what woman wants. Hysterectomy for peri and postmenopausal patients with atypical hyperplasia not receiving estrogens
What is the most common malignancy in the female genital tract?
endometrial hyperplasia
Contrast type I and type 2 endometrial hyperplasias
Type I - peri/post menopause. PCOS type in a way. Good prognosis. PTEN inactivation. Much more common. (endometrioid)

Type II - post menopause. Serous/clear cell. Often poor prognosis. P53 and LOH. Atrophic uteri
Growth pattern of Malignant Mixed Mullerian Tumors
malignant epithelial and stromal elements. Generally elderly women. Highly aggressive.
Mullerian adenosarcoma characteristics
malignant stroma and benign glandular elements. Most occur in postmenopausal women. Indolent growth
What is characterized by islands of endometrial glands and stroma deep within myometrium of hypertrophied smooth muscle?
adenomyosis
What consists of the majority of ovarian neoplasms in children and adolescents?
germ cell tumors
How does age affect [ovarian] germ cell tumors?
children and adolescents 1/3 are benign; adults 95% are benign
What is the most common ovarian germ cell tumor?
Mature cystic teratoma
What are clinical features of immature teratoma?
age <20yo, haphazard arrangement of tissues from all 3 germ layers
What is age of presentation, clinical behavior, and pathologic features of dysgerminoma?
80%< 30yo, 50%< 20 yo, metastasizes via lymphatics to regional lymph nodes, excellent 5 yr survival, large, round nucleus, prominent nucleolus and aggregates of large, uniform cells.

Recurreces treated with XRT. exceellent prognosis if unilateral and encapsulated.
Age of presentation, relevant tumor marker, and clinical behavior of yolk sac tumor [female]
2nd most common malignant germ cell tumor, <30yo, elevated AFP, behavior - locally aggressive, metastasis via lymphatics, hematogenous spread late
Define sex cord stromal tumor
neoplasms derived from granulosa cells, theca cells, Sertoli cells, Leydig cells or fibroblasts. 50% benign fibromas.
Associated hormonal manifestations, microscopic features and recurrence timing for adult granulosa cell tumors
Can rarely be androgenic. Most common clinically estrogenic tumor. More common postmenopausal. May recur 20-30 y later. Coffeebean nuclei. Worse prognosis - higher stage, rupture, large, increase atypia, high mitotic rate
Gross and microscopic features of ovarian fibroma
firm, white gross appearance. micro -intersecting bundles of spindle cells, bands of hyalinized connective tissue. Mean age = 48yo
Contrast Meig's syndrome and Gorlin's syndrome
Meig's = ovarian fibroma, ascites, pleural effusion
Gorlin's - bilateral ovarian fibromas, basal cell carcinoa, jaw keratocysts
Know age at presentation, symptoms, basic microscopic components of Sertoli-Leydig cell tumor (female)
Mean age 25 yo. Symptoms - pain, mass, 30% virilization. Can test Testorerone. Most confined to ovary.
Sertoli areas= hollow or solid tubules
Leydig cells - eosinophilic cytoplasm, pigment, crystals of Reinke
What periods of life are defined by these terms: embryonic, fetal, perinatal, neonatal, and infancy
embryonic - 0 - 10 wks
fetal 10 wks to birth
Perinatal - 20th week to 28d of life
Neonatal - first 28 d of life
Infancy - first year of postnatal life
Major causes of death in neonatal period?
most frequent = congenital anomalies and complications of prematurity
Association of LBW and inadquate perinatal care with increased morbidity and mortality?
higher rates of inadquate care, LBW in african americans. Also see LBW really in younger mothers. Inadequate perinatal care assoc with increased M and M.
What is AGA, LGA, SGA? Understand difference between SGA and LBW?
AGA - birth weight between 10th and 90th percentile for a given gestational age
SGA - birth weight less than 10th percentile for given gestational age
LGA - birth weight greater than 90th for given gestational age

LBW - infant weighing less than 2500 gm
What do preterm? Term? and post-term gestation mean?
Preterm: Birth before 37 wks gestational age
Term: birth at 37-41 weeks
Post-term: birth at or after 42 weeks
Factors associated with SGA?
Maternal factors: HTN, poor nutrition, DM, smoking, substance abuse
Fetal factors: chromosomal, genetic abnormalities, infection
Obstetric: multifetal gestation, abnormal placentation
Factors associated with LGA?
Maternal obesity, excessive maternal weight gain during pregnancy, maternal DM, certain genetic diseases
Major causes of spontaneous preterm delivery?
premature rupture of membrnaes, chorioamnioniits, cervical incompetence, multiparity, multiple pregnancies, uterine anomalies, maternal infection, antepartum uterine bleeding, abruptio placenta, pre-eclampsia
Major diseases/medical conditions of preterm infant?
hyaline membrane disease, BPD, pulmonary and cerebral IVH, PDA, NEC, septicemia, pneumonia, jaundice, kernicterus, retinopathy of prematurity
Importance of organ system maturity and influence on perinatal morbidity and mortality
less mature - higher M and M
Histological changes accompanying lung maturation.
embryonic and psuedoglandular phase - proximal airways, then devo of airways and terminal bronchioles
Cannalicular phase - 17-24 wks - devo of acinus and blood supply
Saccular phase - 24 wks to term - differentiation of epithleium, surfactant production
Alveolar phase - 35 wks on - thin walled alveoli appear and continue to develop
Role of surfactant and why immature lungs are at risk for HMD
decreases alveolar surface tension. Deficiency results in atelectasis, hypoxemia, acidosis, pulm capillary endothelial damage, and intraalveolar fibrin deposition.
Describe HMD in acute phase. Also, What population is at greatest risk?
Lungs are solid, heavy, airless and dark red. Alevoli are collapsed and lined by abundant hyaline membranes which contain fibrin, lipid, and nuclear debris. Infants weighing less than 1000gm, mortality is 50%.
Meaning of RDS and relationship to HMD?
RDS - high RR, labored breathing, cyanosis w/o supplemental O2
Lung radiographic findins - reticulogranular appearance to white lung

HMD is pathologic equivalent to RDS - assoc with male babies, C-section, Maternal DM, AGA, preterm, poor response to O2
What is BPD? change in pathology?
Used to be - babies with positive airway pressure and high O2 tension and then supplemental O2 for 28 d of life. Assisted ventilation and high O2 resulted in chronic fibrosing process in lungs.

Led to HMD and regen stages; then alveolar septal fibrosis and destruction withe emphysematous changes and honeycombing
Now with surfactant = arrest in devo of alveoli - saccules don't divide. Result - fewer, larger alveoli w/decrease in total alveolar septal surface for O2 exchange
Factors associated with pathogenesis of BPD?
prematurity, oxygenation and ventialtion, amnionic infection, nutritional deficiencies, genetic background
What etiology is responsible for the majority of congenital malformations?
Unknown; i.e. idiopathic
What other etiologies are responsible for congenital malformations?
Mutant genes of major affect, chromosome abnormalities, known major environmental factors, multifactorial
What is oligohydramnios? Causes and consequences?
uterine constraint secondary to decreased amount of amniotic fluid. Potter sequence. Decreased urinary output or chronic leakage of amniotic fluid causes oligo. Fetal compression ensues. Consequences: positioning defects, abnormal facies, thoracic and pulmonary hypoplasia, and respiratory insufficiency
How do amniotic bands result in fetal malformation?
disruption and amputation of fetal parts by strands of torn fetal membranes
Which chromosomal abnormality is the most common in live borns?
Trisomy 21
What are the classical manifestations of fetal alcohol syndrome?
dysmorphic facies, growth retardation, CNS (mental retardation)
What are the major pathways of perinatal infection?
ascending (most bacteria, Candida, HSV); hematogenous (most viruses, toxo, syphilis); postnatal (staph, pseudomonas)
What are the outcomes of intrauterine/neonatal infection? Understand that the outcome depends on the organism and timing of infection
can vary from no detectable damage to death to late sequelae
What are indications of FNAB?
Any palpable tumor mass or lesion visualized in any organ
What are contraindications of FNAB?
superficial: uncooperative pt, bleeding diasthesis, uncontrollable cough; suspected carotid body tumor

deep: Bleeding diathesis, seriously impaired lung fcns, suspected vascular lesions, suspected Hydatid cyst, Pheochromocytoma, apprehensive pt
What are sources of error for FNAB Dx?
Inadequate sampling, inadequate processing, erroneous interpretation
Complications of FNAB?
superficial: bleeding/hematoma, local infxn, vasovagal reaction, thyroid issues, pneumothorax

deep: pneumothorax, bleeding/hematoma, peritonitis/pancreatitis/sepsis, air embolism, subQ emphysema
What are dx classification in cytology?
Negative for malignancy, abnormal/atypical cytology (quality) , suspicious for malignancy (insufficient in quantity), Positive for malignancy
Of those women who die from cervical carcinoma, what percentage has had a Pap smear in the last five years?
20%
When should women begin having Pap smear?
Age of first intercourse
How often should a woman get her Pap smears?
every year, then after 3 good ones - every 3 years
What are some of the risks of screening at longer intervals?
loss to follow-up; false negative
Who are considered to be high risk patients for Pap screenings?
early age at first intercourse, multiple lifetime partners or having a male partner with multiple previous partners, smoking, high parity, low SES, immunosuppression, history of STDs, long interval between Pap smears, prior abnormal Pap smears
What is required so that the Pap smear is considered fully satisfactory for evaluation?
ID, clinical information, well visualized, transitional zone seen
What organisms are seen on Pap smears?
trich, candida, HSV, actinomycoses, Gardnarella, chlamydia, pin worm, alternaria
What is the single most important reason for failure of the Pap smear?
failure to get a pap smear
What are the four major areas that contribute to the failure of the Pap smear?
patient related failures, clinical related failures, cytoprep and dx errors, lesion-related errors
What is the major patient-related error for Pap smears?
failure to get a pap smear
What are some clinician-related errors for gyn cyt?
failure to get Pap smear, adequate pap, failing to provide pertinent clin information, failure to follow up, failure to bx suspicious lesions, failure to screen every year
What can contribute to screening and interpretation errors for gyn cyt?
suboptimal staining, failing to detect abnormal slides, decreased conc from screening fatigue, failing to identify slides unsatisfactory for dx, dx errors
What are lesion related errors for Pap smear?
lesions failing to exfoliate, necrosis bleeding or inflamm may obscure or dilute abnormal cells, rapid progression in IC patients. Not a good test for glandular lesions, lymphomas or sarcomas
Pathogenesis for carcinoma for HPV?
progression to CA, high risk DNA integrates into host chromosomes. Disruption of E2 region encoding a transcription regulatory protein. Leads to dysregulation or persistent overexpression of E6 and E7. E6 binds to tumor suppressor p53. E7 binds and inactivates pRB.
What are cervical hyperkeratosis/parakeratosis associated with?
uterine prolapse
What are casues for non-infectious cervicitis?
chemical or mechanical irritation, douching, IUD, diaphragms, pessary
What are clinical points for endocervical polyps?
abnormal bleeding or discharge, multigravidas, 40-60yo
What is Nabothian cyst?
mucus-filled cyst from squamous metaplasia obstructing outlet to cervical gland neck
Where does most CIN arise?
Transformation zone, anterior lip > posterior lip
What is age group of most VIN?
<50yo, not uncommon in 20s and 30s
What are the two types of VIN?
Multifocal with clinical HPV in younger women that doesn't progress.

Unifocal that not associated with clinical HPV that more likely to progress.
What is most AIS associated with?
HPV type 18
What HPV is associated with Invasive Squamous Carcinoma of the cervix?
HPV 16
For invasive cervical squamous cell cancer what are poor predictors?
stage, younger women, overexpression of c-myc or ras
What are characteristics for vulvar squamous cell carcinoma?
older women, burning, pruritus, pain, bleeding, discharge, dyspareunia, observation of a mass
What are the three clinical groups for vulvar squamous cell carcinoma?
1) associated with VIN. Warty or basaloid.Heavy smokers
2) no associated VIN. Older - 77yo.
3) Associated with underlying conditions - DM, CGD
What are prognostic factors for vulvar squamous cancer?
node status, number of positive nodes, bilaterality of nodal mets, extracapsular (nodal) spread
How do 75% of invasive cervical adenocarcinomas present?
abnormal vaginal bleeding
Describe Paget's disease of vulva?
rare form of vulvar intraepithelial neoplasia. chiefly in postmenopausal white women. ~12% associated with invasive adenocarcinoma, protracted course in patients w/o invasion, tendency to recur
What are clinical and pathologic features of solitary follicle cyst?
common in reproductive age. Asymptomatic. Can regress
What are clinical and pathologic features of hyperreactio luteinalis?
Ovarian enlargement caused by numerous luteinized follicle cysts secondary to hCG stimulation

see in conditions with hCG
What are clinical and pathologic features of PCOS?
Idiopathic disorder cx by chronic anovulation, sclerocystic ovarires, inappropriate gonadotropin secretion, hyperandrogenemia and increased peripheral conversion of androgens to estrogens.
sx: obese, oligomenorrhea, infertility, hirsutism

bilaterally enlarged ovaries with numerous small uniform cysts
What are clinical and pathologic features of ovarian torsion?
reproductive age women
What are clinical and pathologic features of tuboovarian abscess?
enlarged cystic mass involving tube and ovary. Manifestation of PID. Acute - intense inflammation with polyps and cell necrosis. Chronic - marked distortion of fallopian tube with occlusion of the lumen, fusion of fimbriae, and tuboovarian adhesions.

PID more common in IUD women
What are clinical and pathologic features of endometriosis?
endometrial epithelium and stroma in ectopic site
Distinguish benign, borderline, and malignant ovarian neoplasms.
benign - single layer of epithelium, no atypia, no mitotic activity, no stromal invasion
low malignant potential - complex papillary projections, stratification of epithelial cells, tufting, mild to moderate nuclear atypia, some mitotic activity, no stromal invasion
malignant - cystic and solid, marked nuclear atypia, high mitotic rate, stromal invasion
Clinical features of serous ovarian neoplasm?
frequently bilateral. Accounts for ~50% of malignant neoplasms. 85% widely disseminated at presentation. They arise from surface epithelial inclusion glands. p53 mutations only with high grade
Clinical features of endometrioid ovarian neoplasm?
1/3 associated with endometriosis: PTEN and LOH. Accounts for 20-25% of neoplasms. 20-25% have synchronous endometrial carcinomas. uncommonly bilateral. Rare spread
Clinical features of mucinous ovarian neoplasm?
jelly belly. uncommonly bilateral. Rare spread.
Clinical features of clear cell ovarian cancer?
association with endometriosis. 50-70% have pelvic endometriosis. Unilocular cyst with fleshy, mural nodules.
Clinical features of Brenner tumor?
benign neoplasm, well circumscribed, coffee bean nuclei
Clinical features of metastatic cancer to ovaries?
Almost always bilateral, multiple nodules
Risk factors for ovarian cancer?
nulliparity, difficulty conceiving, industrialized citizen, never used OC, family history
Stage and ovarian cancer?
Stage is most important prognostic factor. About 75% of pts with ovarian cancer present with stage III or IV disease
Describe the major congenital anomaly of the testis?
Cryptorchidism. 3% of full-term males. 75% descend w/in 3 months. Undescended testis more prevalent in preterm, SGA, LBW, and twins. Higher risk for testicular neoplasia .Also hernia, torsion, and infertility.

2y - arrest in germ cell devo and atrophy
Describe types of inflammation and infection that can involve the testis
Nonspecific testicular inflammation- usu bacterial UTI from epididymis
Granulomatous orchitis - unilateral testicular enlargement
Gonorrhea - epididymis first. maybe abscess
Mumps - after parotitis, then painful swelling
TB - epididymis primary site
Syphilis - testes first
What are clinical and morphological findings in testicular torsion?
venous infarction. Usu males 12-20yo. Trauma can precipitate, often underlying abnormality like incomplete descent, absence of scrotal ligaments or testicular atrophy
What are the clinical aspects of testicular neoplasms?
Most common cancer in young men 15-35. Common - Scandinavia, Switzerland, Germany, and NZ.

Risk factors - cryptorchidism, prior testicular germ cell tumor, family Hx, gonadal dysgenesis, Androgen Insensitivity Syndrome

Ages
children - yolk sac tumor
men - seminoma and mixed germ cell
old - lymphoma
5% gynecomastia
What is succenturiate lobe?
one or more discrete lobes is separated from main placental mass. Vascular supply reaches accessory lobe by runnin through fetal membranes unsupported by underlying villous tissue.
Complications: vessel rupture during delivery - fetal blood loss
Retention of lobe
What are the placenta cretas?
Increta. Accreta. Percreta.
What are the placentation types?
dichorionic and diaminonic with separate placentas or fused placentas.
Monochorionanic diamnionic
Monochorionic monoamnionic

All dizygous twins are dichorionic
What are the two forms of placental inflammation and infection?
Ascending. Incidence inversely proportional to gestational age. See acute chorionaminonitis.

Hematogenous. Generally Viral or syphilis/listeria. See villitis.
What are umbilical cord anomalies?
Single Umbilical Artery (associated with fetal malformations, LBW. Insertion (Velamentous) = insertion into membranes. Complications during delivery, fetal blood loss.
What is meconium stain?
Due to meconium passage in utero. Engulfed by macs in fetal membranes
What is amnion nodosum?
Amnion studded with small nodules composed of cellular debris. Associated with oligohydramnios.
What is amnionic band syndrome?
Strings of detached amnion entangle limbs, digits, UC constriction, amputation defects
What is pregnancy induced hypertension related changes?
Changes small villi, syncytio knots, acute atherosis of spiral arteries
What are forms of gestational trophoblastic disease?
Mole. Choriocarcinoma. Placental Site trophoblastic tumor