WomensHealth_Test2 Word Scramble
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Question | Answer |
Pre-conception care always think... | BMI!!! Age, Hx, Meds, FH, substance abuse, diet |
During physical exam for preconception care what should you check for? | Dental Caries |
During labs for preconception care what should you check for? | Rubella, varicells, HepB, HIV, RPR, CBC, G/C culture |
Which immunizations can you NOT give if pregnant? | MMR & Varicella |
How much folic acid pre-pregnancy? | .4-.8mg daily _4mg if hx of neural tube defects |
When is 1st visit recommended? | ~6-8 wks gestation |
Gravida-v Para- w x y z | v=# pregnancies w=# full term births x=# pre-term births (<37wks) y=# abortions (spont, induced, ectopic) z=# living children |
How would you calculate estimated date of confinement (EDC=Delivery Date)? | Add 7 days to LMP and subtract last month: LMP: 2/20/11 then EDD=11/27/12 |
Blue/purple coloration of cervix/vagina | Chadwick's Sign |
Palpable softening at isthmus | Hegar's Sign |
What MUST you do on physical exam for 1st prenatal visit? | Pap smear, Chlamydia/Gonorrhea Swab |
Additional labs for women @risk | TB, HepC, Varicella, Trich Vaginalis, HSV, Hgb A1C |
What's absolutely necessary to perform at the first prenatal visit | Ultrasound to confirm pregnancy |
When is the second trimester? | Week 13-end of 26 |
When is the third trimester? | Beginning of week 27 |
How many times should she visit in the first 28 weeks? (1st and 2nd Trimester) | Every four weeks |
How many times should she visit in wks 28-36 | Every two weeks |
The first fetal movements (if first pg usually @18-20wks) | Quickening |
After the first visit, what should you begin monitoring? | BP Fetal Heart Tones (120-160bpm norm) Fundal height Extremities |
In third trimester what should you do to see the position of the head? | Leopold Maneuvers |
In third trimester why check the cervical exam? | For: Dilation Effacement Station Presenting Part |
Station 0 of head | Head is @bony ischial spines & fills the maternal scrotum |
Negative Stations of head | Number of cm head is above the ischial spines |
Positive stations of head | Number of cm head is below the ischial spines |
What should you test for at every visit?? | Urine for protein & sugar _Test for CBC in early 3rd trimester to assess for anemia |
When should you screen for gestational diabetes? | At 24-28wks _>1 abnormal value is sign after 75g 2hr oral glucose tolerance test |
During initial labs you use this and then test again in the third trimester. If this tests NEGATIVE then should give Immunoglobulin at 28-30wks | Rhogam _Rh Immune Globulin 300ug |
When should you test for GrpB strep (swabbing both lower vagina & rectum). | Btwn 35-37wks (right before delivery) _If +, need intrapartum Abx prophylaxis to decrease incidence of neonatal GBS |
When can you offer aneuploidy screening? | At <20wks |
1st Trimester Combined Test for Aneuploidy (Down's) | Performed 11-13wks w/nuchal translucency w/serum markers |
1st Trimester Quad Screen for Aneuploidy (Down's), Neural Tube Defects, Trisomy 18 | Maternal serum screen _Can perform @15-18wks (as late as 22wks) _AFP _hCG _uE3 _Inhibin A |
In the 1st trimester, why do an obstetric ultrasound? | For dating purposes, to ck for bleeding or pain, locate pregnancy location |
In the 2nd trimester, why do an obstetric ultrasound? | Fetal growth, anatomy survey, placenta location _@18-20wks _Level 1:Basic _Level 2:In Depth Determine future sex |
In the 3rd trimester, why do an obstetric ultrasound? | Fetal growth, presentation, bleeding _Biophys Profile |
During the 3rd trimester do a biophysical profile to check for what? | Fetal movement, tone, breathing. Amniotic Fluid Volume Results of nonstress testing |
Recommended weight gain for BMI <18.5 during pregnancy (underweight) | 28-40 lbs |
Recommended weight gain for BMI 18.5-24.9 during pregnancy (normal weight) | 25-35 lbs |
Recommended weight gain for BMI 25-29.9 during pregnancy (overweight) | 15-25 lbs |
Recommended weight gain for BMI >30 during pregnancy (obese) | 11-20 lbs |
Tests for fetal well-being | Fetal movement/Kick counts Non-stress Test (NST) Contraction Stress Test (CST) Biophysical profile |
Antiemetics used for N/V during pregnancy | Phenergan, Compazine, Reglan, Zofran, Ginger |
Uterine activity that results in progressive dilation & effacement of the cervix | Labor |
Thinning/shortening of cervix length. Normal is >2.5cm | Effacement |
Diameter of cervical os in centimeters. Complete=10cm dilation & 100% effacement | Dilation |
Regular intervals, gradually increasing in frequency. Increasing intensity; cervical dilation, back/ab pain, no sedational relief. | True Labor |
Irregular intervals & duration of contractions, intensity NOT changed, no cervical dilaiton, low ab pain, can relieve w/sedation | False Labor |
Pooling of amniotic fluid in vagina or direct visualization of fluid leaking through cervix may support this | Membrane Rupture _Leaks amniotic fluid _Nitrazine Test: Intact pH-5-6 Ruptured pH6.5-8 *blue |
Fern test would show what? | Amniotic fluid status (if dry, will have fernlike pattern) |
Interval btwn labor onset & full cervical dilation & effacement. | First stage of labor |
Begins with first regular contraction & ends at 3-4cm. Rate of dilation is slow ~.5cm/hr | Latent phase in the first stage of labor |
Follows the latent phase (of first stage of labor) with rate increasing to ~1cm/hr. Ends with complete dilation | Active phase in the first stage of labor |
Begins w/complete dilation & ends with infant delivery. Entails the "pushing" phase of birth | Second stage of labor |
Delivery of infant & ends with delivery of placenta | Third stage of labor |
Uterine contractions will increase in freq/strength in the POWER PROGRESS of labor. will lead to increased sensitivity of uterine m fibers to oxytocin. What causes initial change? | Prostaglandins E2 & F2alpha |
During the power phase, what is the adequate labor of uterine contractions | 3-5 contractions in 10min |
measures frequency and duration of contractions, but not intensity | External tocodynamometry |
Measures frequency, duration AND intensity of contraction via IUPC (intrauterine pressure catheter) | Internal tocodynamometry |
Macrosomic Infant | >4500 grams _Large infants |
Relation of the fetal presenting part to the right or left side of the maternal pelvis | Position |
Bounded by the symphysis (top), sacral promontory (posterior), & pectinate lines (lateral) | Inlet part of bony pelvis |
Midpoint of symphysis (top), midpoint of sacral curve (posterior), & ischial spines (lateral) | Midpelvis part of bony pelvis |
Inferior border of symphysis (anterior), tip of sacrum (posterior), ischial tuberosities (lateral) | Outlet part of bony pelvis |
Most common, best suited for childbirth | Gynecoid position |
Occiput posterior presentation | Anthropoid |
Most UNFAVORABLE position for delivery | Android |
Least common type of delivery | Platypelloid |
Passage of the widest diameter of the presenting part to a level below the plane of the pelvic inle | Engagement |
#2 Flexion | With the head completely flexed, the fetus presents the smallest diameter of its head |
#3 Descent | Greatest rate of descent occurs during the latter portions of 1st stage of labor and during 2nd stage of labor |
#4 Internal Rotation | Rotation of presenting part from its original position (usually transverse) to anteroposterior position as it passes through the pelvis |
#5 Extension | Occurs once fetus descends to level of introitus; head will extend beneath maternal pubic symphysis & head delivers |
#6 External Rotation (Restitution) | The head rotates 45 degrees to line up with shoulders which are oblique in maternal pelvis |
Uterus rises in abdomen, globular configuration, gush of blood and/or lengthening of umbilical cord | Third Stage of Labor _Placental delivery |
Baseline Rate of Fetal Heartrate | 120-160 _>180 severe tachy _<100 severe brady |
Fluctation in HR with changing amplitude in every beat | Short term variability |
Wavelike pattern that changes 4-6 cycles/min | Long term variability of HR |
Acceleration, increases 15bpm above baseline & lasts 15 seconds | Periodic changes in fetal HR |
Mirrors shape of contraction. Due to head compression. Physiologic. | Early deceleration of HR |
With respect to timing of contraction, shape & severity. Caused by cord compression | Variable deceleration in HR |
Caused by fetal HYPOXIA, placental insufficiency, maternal HYPOtension or hypoxia | Late deceleration in HR |
Short term variability with long term variability present in fetal heartrate | Normal fluctuation |
Lamaze, relaxation techniques | Psychoprophylaxis |
Sedatives (Vistaril), Narcotics (Demerol, Stadol, Nubain), Dissociative Drugs (Ketamine) | Systemic Drugs during labor |
Paracervical block, pudendal block, epidual | Labor Pain Relief |
Perineal laceration involving only skin & vagina | 1st degree perineal laceration |
Perineal laceration involving skin, vagina & deeper perineal tissues | 2nd degree perineal laceration |
Perineal laceration involving external anal sphincter & skin, vagina & depper perianal tissues | 3rd degree perineal laceration |
Perineal laceration involving rectal mucosa, external anal sphincter,skin, vagina & depper perianal tissues | 4th degree perineal laceration |
9-13 points on Bishop score | High likelihood of successful induction of labor |
0-4 points on Bishop score | High likelihood of failure with induction of labor |
Stripping membranes, amniotomy, PGE gel, oxytocin, Cytotec | Induction of labor |
Complications of oxytocin | 1)Uterine Hyperstimulation: >5 contractions every 10 minutes 2)Fetal distress/intolerance to labor: LATE decelerations of fetal HR 3)Water intoxication: caused by antidiuretic properties of oxytocin |
Period following delivery of baby & placenta to about 6 weeks postpartum. | Puerperium _Anatomy resolves: uterus involutes, cervix loses marked vascularity/glandular hypertrophy/hyperplasia, ovarian function(lactating influenced by prolactin. While lactating, no ovulation). Vaginal vault will decrease in size. |
How long hospitalize after birth? | Natural: 1-2days C-Section: 2-4days |
Autoab's attack ECM & basement. Affects all levels of skin. 22% genetic. _Trauma: Kobner's phenom (possible) _Contact dermatitis | Lichen Sclerosus _POST Menopause _Pruritis _Dysuria, Dyspareunia(painful sex) |
Itchy "cellophane paper" waxy/hyperkeratotic WHITE plaques. See purpura, erosion, fissures. (NOT seen where there is keratin, hair or mucous membranes) | Lichen Sclerosus _Menopausal women _On vestibule, vagina, rectal mucosa |
Left untreated this disease which causes cellophane waxy white plaques may cause squamous cell carcinoma. | Lichen Sclerosis _At risk of old or HYPERkeratotic lesions _May be HYPOthyroid |
Labs for dx of Lichen Sclerosus (itchy cellophane paper waxy keratin plaques) | Vulvar Punch Biospy |
Tx of of Lichen Sclerosus (itchy cellophane paper waxy keratin plaques) | TOPICAL Ultrapotent Steroid OINTMENT _Temovate!! |
Cysts form here as result of obstruction caused by trauma or inflammation. Abscess forms from infected cyst or primary gland infection (polymicrobial or STI) | Bartholin Cyst (in labia minora) _Acute, painful UNILATERAL labial swell _Painful sex, pain when sitting/walking _Tender, fluctuating mass that's red/swollen w/cellulitis. _May see FEVER associated w/infection |
Tx of Bartholin cyst | Incision/drainage with Word Catheter _Culture the pus _Empirically give Keflex or Doxy _Sitz baths 2-3dd after I&D _NO SEX till remove catheter |
Neoplastic cells in squamous epithelium. | Vulvar Intraepithelial Neoplasia (VIN) _Only VIN 2/3 are true precursors to vulvar cancer |
Associated with HPV 16 & 18. Usual type. See in young women. Risk: smoking, immunosuppresion, many sex partners | Vulvar Intraepithelial Neoplasia Usual(VINu) Dx: Vulva Colposcopy (acetic acid, lesions will change color from gray to white or red to black) _Typically NO sx _Often associated with cervical intraepithelial neoplasia, therefore MUST perform colposcopy |
When should you biopsy a VIN (vulvar intraepithelial lesion) | If has pigment |
Treatment of VINu (vulvar intraepithelial lesion-usual) with medication | All are OFF-LABEL; none really guarantee cure -5FU (Efudex) -Interferon (Intron-A) -Imiquimod (Aldara) |
Standard of care tx of VINu | Surgical Tx: CO2 laser vaporization (destroys entire epithelium) Local wide excision Vulvectomy Post-Tx Rate: 30-50% |
NOT associated with HPV. Differentiated, effects older women >70, involves LOWER 1/3 of epithelium ONLY | VINd (vulvar intraepithelial lesion-differentiated) _Associated w/sqaumous cell hyperplasia (Lichen's...) _Prevention: Tx of underlying condition _Tx: Surgery |
Post-treatment of VIN | Colposcopy vulvar inspection at 6mos, 12mos and then annually. |
Most common symptom of vulvar cancer | Pruritis _Usually asymptomatic, therefore INSPECT THE VULVA |
Varies in appearance from large, exophytic, cauliflowerlike lesion to small ulcerative lesion with lesion to small ulcerative lesion with surrounding hyperkeratosis | Squamous cell carcinoma in vulva |
Raised lesion w/ULCERATED center & rolled borders | Basal Cell carcinoma in vulva |
Seen @labia minora & clitoris. Raised DARK pigment lesion | Malignant Melanoma on vulvar cancer |
Tx of vulvar cancer | Surgical removal with inguinal node dissection (radiate if lymph involved) |
HPV must be present in order to develop this neoplasm. May have NO history of cervical cancer/neoplasms. | Vaginal Intraepithelial Neoplasia (VaIN) _In UPPER 1/3 of vagina _Usually preceded by sqaumous carcinoma of vulva or cervix _At risk if have hx of CIN III |
Benign Viral proliferation of VaIN | VaIN 1 (Vaginal Intraepithelial Neoplasm-1) _Observation with cytology/HPV/Colposcopy every 6months |
Intermediate risk of proliferation of VaIN | VaIN 2 (Vaginal Intraepithelial Neoplasm-2) _Surgery +/- chemo |
True precursor to vaginal cancer | VaIN 3 (Vaginal Intraepithelial Neoplasm-3) _Surgery +/- chemo |
Detection of VaIN (Vaginal Intraepithelial Neoplasm) | Pap Smear (cytology) Colposcopy |
When would you perform a vaginectomy when dealing with VaIN (Vaginal Intraepithelial Neoplasm) | Suspect invasion, >40, cytology & colposcopy differ & if extended sampling is needed. _Will remove UPPER 1/3 of vagina (90%success) -SE: shorter vagina, blood loss, skin graft, poor sexual functioning |
Used to destroy dysplastic cells to 1.5mm depth but unable to assess lesions extending into vault or lesions within surgical scar from TAH & operator dependent | Laser Vaporization |
Topical chemo used for VaIN tx _ONLY use if other tx NOT available! | 5FU (50-85% success). Causes vaginal epithelium to slough. _ONLY used if other tx options NOT feasible! |
Most common reason for vaginal cancer | Metastasis from endometrium, ovary or cervix _ONLY when PRIMARY site is from vagina can you call it vaginal cancer _<20% dx under 50 _Squamous Cells MOST common |
Most common cell type in vaginal cancer | Squamous cell |
Milky discharge, vaginal odor & post-sex bleeding are signs of this | Vaginal cancer _Since so rare, no standard tx _Combo: vaginectomy & radiation |
MOST common type of ovarian cyst. NON-malignant. Will regress after 1-2 menstrual cycles. | Follicular Cyst _Mature follicle won't rupture OR _Non-dom follicles will not die in presence of Graafian |
NON-resorption of blood from the cavity of the corpus luteum (>3cm) called this. Will resolve after 1-2 menstrual cycles | Corpus Luteum Cyst |
This cyst, seen with INC chorionic gonadotropin levels is typically seen bilaterally. Fluid is clear, straw-colored. _Hydatidiform Mole _Choriocarcinoma _Clomid Therapy for infertility | Theca Lutein Cyst _Will regress if tx underlying disorder |
Half of all benign neoplasms are this. Come from germ cells & found along migration pathway of germ cells-->glands. | Mature Teratoma _Will see well-differentiated tissue from any of 3 germ layers (ectoderm, mesoderm, endoderm) _Cyst lined with keratined squamous epithelium w/abundant sebaceious & apocrine glands _USUALLY ectodermal origin: hair, teeth |
This cyst doesn't typically have sx unless secondary to torsion or rupture. Have urinary frequency/urgency. See back pain. Will feel a pelvic mass on bimanual exam. | Mature Teratoma _Will see well-differentiated tissue from any of 3 germ layers (ectoderm, mesoderm, endoderm) _Cyst lined with keratined squamous epithelium w/abundant sebaceious & apocrine glands _USUALLY ectodermal origin: hair, teeth |
Dx of Mature Teratoma _Will see well-differentiated tissue from any of 3 germ layers (ectoderm, mesoderm, endoderm) _Cyst lined with keratined squamous epithelium w/abundant sebaceious & apocrine glands _USUALLY ectodermal origin: hair, teeth | Transvaginal ultrasound (unilateral, COMPLEX cyst) CEA, CA-125, AFP, bHCG (all should be within normal) |
Tx of Mature Teratoma _Will see well-differentiated tissue from any of 3 germ layers (ectoderm, mesoderm, endoderm) _Cyst lined with keratined squamous epithelium w/abundant sebaceious & apocrine glands _USUALLY ectodermal origin: hair, teeth | Lapartomy/Laparoscopy Ovarian cystectomy/oophorectomy _10% chance of recurrence |
Highest incidence among women 65-74 | Ovarian Cancer _2nd most common gyno cancer |
Incessant Ovulation Theory of Ovarian cancer | Repeated ovarian epithelial trauma by follicle rupture & subsequent epithelial repair causes genetic change within surface epithelium |
Gonadotropin Theory of Ovarian cancer | Persistent stimulation of ovaries by gonadotropin coupled w/local effects of endogenous hormones. INC surface epithelial proliferation & subsequent mitotic activity. |
Reduce risk for ovarian cancer | Multiparity Breastfeeding Long-Term OCC use Bilateral Tubal Ligation Low Fat Diet |
Serous epithelial neoplasm in OVARIAN cancer | From fallopian tube _MOST common type!!! |
Mucinous epithelial neoplasm in OVARIAN cancer | From cervix |
Clear cell epithelial neoplasm in OVARIAN cancer | From mesonephros _<1% _Rarely reach size of serious/mucinous neoplasms _Bio AGGRESSIVE _HYPERCalcemia & HYPERpyrexia |
Neoplasm from germ cells, 20-30yo, grow rapidly, favor lymphatics & contain mix of tumor types. Typically unilateral. | Germ Cell Neoplasms in Ovarian Cancer _Produce helpful tumor markers |
Dysgerminoma, endodermal sinus tumor, immature teratoma, embryonal carcinoma & choriocarcinoma | Subtypes of Germ Cell Neoplasms in Ovarian Cancer |
MOST common type of germ cell neoplasm | Dygerminoma _Unilateral _<30 |
Bilateral germ cell tumor with MOST RAPID growth. Makes AFP | Endodermal Sinus Tumor |
2nd most common type of germ cell neoplasm seen typically under 20. Makes AFP | Immature Teratoma |
Uncommon germ cell tumor with rapid growth & EXTENSIVE SPREAD. Makes AFP AND HCG | Embryonal Carcinoma |
Germ cell neoplasm seen with precocious puberty, uterine bleeding or amenorrhea. VERY RARE. 20's | Choriocarcinoma |
MOST common type of sex-cord stromal tumor. Causes HYPERestrogenism (precocious puberty, post menopause bleeding). In 50s. | Granulosa Cell _Sex-Cord Stromal Tumors |
Rare sex-cord stromal tumor that causes HYPERandrogenism. See in 30-40. | Sertoli-Stromal cell _Sex-Cord Stromal Tumor |
No sx until advanced, Nausea, dyspepsia, changed bowel habits, ab distension, pelvic pressure, abnormal vaginal bleeding, wt loss | Ovarian Cancer _Ascites, Inguinal Lymphadenopathy, Pelvic mass |
When would you order CA-125? | Suspect EPITHELIAL ovarian cancer >65U/mL |
When would you order hCG, AFP, LDH | Suspect GERM cell tumor |
Only 2 germ cell tumors to for sure show hCG | Choriocarcinoma Embryonal Carcinoma |
Only 2 germ cell tumors to definitely NOT show AFP | Choriocarcinoma Dysgerminoma |
Tx of Ovarian Cancer | Consult gyno oncologist Surgical Staging Chemo |
Uncontrolled androgens/metab will INC testosterone, androsterendione, DHEA-S. Will see INSULIN-RESISTANCE & HYPERinsulinemia because insulin changes FSH/LH effects on ovarian function. Will DEC synthesis of SHBG & IGF1. Will see DEC Adiponectin. | Polycystic Ovarian Syndrome _Ovarian Androgen EXCESS |
Under INC levels of insulin androstenedione what happens to androgens? | Androgens converted to testosterone instead of estrogen. This will INC SHGB but because of already high insulin levels, production will be decreased, causing INC in free testosterone. |
Infertility, anovulation, obesity, acne, hirsutism, male-pattern baldness, acanthosis nigricans, metabolic syndrome, sleep apnea | Polycystic Ovarian Syndrome _Ovarian Androgen EXCESS |
What must you rule out before you dx female with Polycystic Ovarian Syndrome _Ovarian Androgen EXCESS | HYPERprolactinemia CAH Cushings --After rule out, THEN must have 2 of 3: oligomenorrhea, HYPERandrogenism, polycystic ovaries |
What would you expect to find on ultrasound of Polycystic Ovarian Syndrome _Ovarian Androgen EXCESS | >12 follicles in each ovary (2-9mm) String of Pearls appearance Ovaries >10ml |
What lab would be a good indicator of Polycystic Ovarian Syndrome _Ovarian Androgen EXCESS | LH: FSH will =3:1 |
Tx for Polycystic Ovarian Syndrome _Ovarian Androgen EXCESS | Weight Loss (INC SHGB, dec testosterone) Metformin (only if have HYPERinsulin) Combined Oral Contraceptives Fertility consult Provera (protects endometrium) Lifestyle modification |
Risks associated with Polycystic Ovarian Syndrome _Ovarian Androgen EXCESS | Endometrial Hyperplasia/Carcinoma Type2 DM HTN High Cholest Cardio Dz Stroke |
Bartholin glands are located where? | At 4 and 8 o'clock position of labia minora |
Most common cause of vaginal cancer | Metastasis |
Stratified squamous epithelium in cervix | Exocervix |
squamo-columnar junction & metaplastic squamous epithelium in cervix | Transformation zone of cervix |
Single layer mucin-producing columnar cells in cervix | Endocervical canal |
HPV will infect which level first before remaining latent, then activated by immune deficiency | Basal Layer _mature basal cells containing HPV will migrate from basement membrane to surface |
High risk type of HPV | HPV 16 & 18 |
Low risk type of HPV | HPV 6 & 11 |
Will long-term COCs put you at risk for HPV? | Yes, COCs are a risk factor for HPV infection |
When should you begin screening for HPV | Begin at 21 |
When should you begin performing PAPs? | NEVER before 21 |
When should you stop screening for cervical cancer? | Between 65-70 if last 3 consecutive PAPs were normal & no abnormal PAP in the last 10 yrs and no HSIL in last 20yrs |
When should you stop screening for cervical cancer after hysterectomy? | If hysterectomy was for BENIGN reasons, can stop screening |
How often should you screen for cervical cancer? | Every 2 yrs |
When should you do Cytology + HPV DNA? | In Women >30 _If DNA is neg, repeat every 3yrs until 45 |
BEST screening test for cervical cancer | HPV DNA |
Receive results with negative HPV DNA. What does this say about the cytology? | NORMAL cytology |
Receive results with positive HPV DNA. What should you do? | Refer for colposcopy |
Causes of atypical cells of undetermined significance, NOT HPV: | Chlamydia Trach HSV Vulvovaginal Atrophy |
See low-grade squamous intraepithelial lesion(HYPERchromatic w/INC cytoplasm) What should you assume? | That there's HPV DNA _Refer for Colposcopy!! |
Large cell with INC cytoplasm. Hyperchromatic nuclei | Low-grade squamous intraepithelial lesion |
Large cell with DEC cytoplasm. Hyperchromatic nuclei | High-grade squamous intraepithelial lesion _Assume +HPV and refer for colposcopy |
What should you do for cytology that may suggest intraepithelial lesions in adolescents? | Repeat cytology in 12 months. Remember do NOT give PAP till 21!! _2 positive results, refer for colposcopy |
Why should you differentiate between transient & persistent HPV infection (+HPV but NEG cytology). Repeat in 12 mos. | Persistently +HPV puts at risk for devo of cervical intraepithelial neoplasia |
Woman with endometrial cells on PAP & menopausal. Next step? | Transvaginal US +/- endometrial biopsy |
What does it mean to see endometrial cells on PAP? | Functioning endometrium Benign endometrium w/stromal breakdown Hormone alteration & endometrial cancer |
Cervical lesion in LOWER 1/3 of epithelial lining | CIN 1 (Cervical Intraepithelial Neoplasm) _Typically regress in 1yr |
Cervical lesion in LOWER 2/3 of epithelial lining | CIN 2 (Cervical Intraepithelial Neoplasm) _half regress, a quarter progress |
Cervical lesion with >2/3 of epithelial lining | CIN 3 (Cervical Intraepithelial Neoplasm) |
Biopsy confirmed CIN1 (lower 1/3 epithelium) | EXPECTANT management _Repeat cytology/HPV test in 12 months _If still abnormal, refer for colposcopy _Lasts >1 yr, can excise |
Biopsy confirmed CIN2/3 (involves lower 2/3 epithelium) | Tx!! _Cryotherapy or LEEP _REMOVE transformation zone (this only removes the cells, NOT the HPV virus!) |
Destroys tissue @transformation zone in cervical neoplasm by NO2. | Ablative Therapy _Disadvantage: Cannot do histo on tissues _NO invasion, PG, HIV |
After effects of Ablative Therapy | Vasomotor response during procedure Cramp Profuse, bad smelling WATER discharge Infection/Bleeding (<5%) Cervical Stenosis (<5%) |
What determines success rate in ablative therapy? | SIZE of lesion (not the grade). Lesions at 3 and 9 oclock have INC blood supply therefore may RESIST the cooling temp. |
High electrical current density-->rapid heating of tissue for cervical dysplasia. Tissue IS ABLE TO SEND to Histo. | Loop Electrosurgical Excision Procedure _Has replaced Laser surgery! |
Precursor to cervical cancer. Has endocervical gland involvement which is lined w/atypical columnar epithelial cells. | Adenocarcinoma in situ _Hard to manage since may be in canal & may have skip lesions |
Why might you have delayed dx of Adenocarcinoma in situ | Cytology better at seeing SQUAMOUS than Glandular disease (which is adenocarcinoma) _MUST perform Endocervical Curettage during colposcopy |
A large area of tissue around cervix is excised for exam | Cold Knife Colonization |
Gardasil protects against which type of HPV | 6, 11, 16, 18 (Quadrivent) |
Cevarix protects against which type of HPV | 16 & 18 (Bivalent) |
This type of cervical cancer is DECREASING. Is microinvasive/invasive | Cervical Squamous Cell Cancer |
This type of cervical cancer is INCREASING | Cervical Adenocarcinoma _Endocervical, Endometroid, Clear Cell, Adenoid Cystic |
HPV 16 typically causes this type of cervical cancer | Squamous cell (50-60% of the time) =16SS |
HPV 18 typically causes this type of cervical cancer | Adenocarcinoma (40-60% of time)...ON the rise _=18A |
Columnar cells with ELONGATED nuclei that are large, hyperchromatic. See MITOSIS & APOPTOTIC bodies | Cervical Cancer |
Typically no sx but may see vaginal bleeding (MOST common), after sex bleed, pelvic pain that unilaterally radiates (sign of advanced dz), and vaginal discharge | Cervical Cancer |
If patient with cervical cancer has pelvic pain that's unilateral with radiation to hip thigh, thoughts? | Late Stage Cervical Cancer |
Arise from smooth m cells in uterine walls. Made of collagen, smooth m, elastin surrounded by pseudocapsule. MORE common in black women (age 50) | Uterine Fibroids |
Does estrogen cause myomas (uterine fibroids)? | Estrogen does NOT cause myomas, but does encourage their growth. Have higher amt of receptors and estrogen may cause INC ECM growth. |
Lies just beneath endometrium | Submucosal uterine fibroids |
Lies just at serosal surface of uterus | Subserosal uterine fibroids |
Lies within the uterine wall | Intramural uterine fibroids |
50 y/o black woman with abnormal uterine bleeding, pain w/contraction, pelvic pressure, infertile & spontaneous abortions | uterine fibroids |
Saline-Infused sonohystgram & hysteroscopy can help show this | uterine fibroids |
GnRH agonist that decrease fibroid size. Improves anemia before surgery, allows minimal invasive. Do NOT use >6mos!! | Depot Lupron |
For patients w/prolonged, heavy menses with NO submucosal fibroids | Steroidal therapy OR Lysteda (oral antifibrinolytic): use ONLY during menstrual cycle |
Preserves fertility/uterus and can be performed on ALL types of uterine fibroids. | Myomectomy |
When can you perform an abdominal or minilaparotomic myomectomy? | Contraindic for laproscopy (cardiopulm dz or fibroids too big) Prior pelvic/ab radation severe hip dz DEC BMM, renal, liver fcn |
Preserves fertility/uterus. ONLY performed on SUBMUCOSAL fibroids | Hysteroscopy _Use heated loop to resect _May cause fluid overload & HYPOnatremia |
Minimally invasive for fibroids but no future kids! MUST continue a contraceptive too. Only use if NO distorsion (remove fibroids first) | Endometrial Ablation _Destroys endometrium |
Preserves uterus but NOT fertility to tx fibroids. Embolize uterine a to cut off blood supply to fibroid | Uterine a Embolization _NO future kids!! _No numerous/large fibroids! |
Presence of endometrial glands & stroma outside endometrial cavity & uterine muscles. Usually in pelvis. | Endometriosis _Premenstrual pelvic pain, infertility, painful periods/sex, INC CA-125 |
MOST common dx for hospitalizing women 15-44 | Endometriosis _INC risk of ovarian cancer _Premenstrual pelvic pain, infertility, painful periods/sex, INC CA-125 |
Retrograde menstruation, deficient cellular immunity (INC risk of AI disorders) & hereditary play risk in this dx | Endometriosis _Premenstrual pelvic pain, infertility, painful periods/sex, INC CA-125 |
Premenstrual pelvic pain, infertility, painful periods/sex, INC CA-125 | Endometriosis |
Why is their premenstrual pelvic pain in endometriosis? | Lesion grows w/estrogen & progesterone but their expansion is stopped by surrounding fibrosis-->pressure & inflammation leading to pain which will subside after menses. |
Tender at posterior cul-de-sac. Fixed or retroverted uterus. Adnexal masses or tenderness | Endometriosis _Premenstrual pelvic pain, infertility, painful period/sex, INC CA-125 |
Dx of endometriosis | Laparscopy: Red petichial lesions on peritoneal surface. Surrounding peritoneum is thick & scarred. Ovaries show lesions or chocolate cysts. See adhesions. |
Red petichial lesions on peritoneal surface. Surrounding peritoneum is thick & scarred. Ovaries show lesions or chocolate cysts. See adhesions. | Endometriosis _Chocolate Cysts & red petichia on peritoneum |
Tx of mild endometriosis | NSAIDS |
Tx of mod-severe endometriosis | Goal: STOP endometrial tissue stimulation -OCPs -Progestins -Deopot Lupron _Laparscopy w/fulguration _hysterectomy w/bilat salping-oophorectomy |
MOST common pelvic genital cancer | Endometrial Cancer _Early menarche, late menopause, OBESITY!!! |
Huge cause for endometrial cancer | OBESITY!! |
Cause of endometrial cancer | INC estrogen levels which stimulates proliferation of endometrium. Unopposed will cause endometrial hyperplasia & atypia. |
Cancer which arises due to UNOPPOSED endog/exog estrogen. Has FAVORABLE prognosis bc well-differentiated tumor | Type 1 Endometrial Cancer |
Arises independently of estrogen & seen with endometrial atrophy. Poorly differentiated therefore poor prognosis. | Type 2 Endometrial Cancer |
MOST common type of endometrial cancer | Adenocarcinoma |
Endometrial cancer NOT associated with HYPERestrogen state. Poor prognosis | Serous Carcinoma or Clear Cell (High grade, aggressive with deep invasion) |
Most common stage of endometrial cancer found | Stage 1 Endometrial Cancer |
Abnormal vaginal bleeding, ab cramping, back pain, weight loss, painful sex. Screen if have hereditary nonpolyposis colon cancer syndrome (HNPCC) | Endometrial Cancer |
Pap smear with endometrial cells may show this | endometrial cancer |
May cause endometrial cancer | Tamoxifen |
Tx of endometrial cancer | Hysterectomy with bilateral salpingoophorectomy w/pelvic & periaortic lymphadenectomy Radiation (if surgery contraindications) Chemo (RARE, only if advanced dz) |
32 yo female presents for her WWE visit and you see she had (-) cytology but (+) HPV DNA on last years Pap. This year cytology remains negative but HPV DNA is still (+). What do you recommend? | Refer for Colposcopy with 2 positive HPV tests |
When should you offer a colposcopy? | With 2 consecutive year HPV + results. |
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