ObGyn Chapter 1: The Womens Health examination 1) Medical History a) CC, ROS, Past Hx, Family Hx, and

Social Hx 2) Gynecologic History a) Menstrual History i) Last menstrual period ii) Length of periods iii) Number of days in between periods iv) Any recent changes in periods v) Flow during periods vi) Clots during periods b) Menstrual pain i) Prostaglandin mediated and should be relieved by NSAIDS ii) Use FARCOLDERS when evaluating pain c) Definitions i) Menopause: 1 year after menses have ceased ii) Perimenopause: transition from menstrual to non-menstrual function may last 1-2 years d) Sexual history i) Please tell me about your sexual partner, or partners? ii) Currently sexually active or not? iii) Number of partners iv) Partners gender v) Methods of contraception and STD protection 3) Obstetric History a) Gravidity and Parity i) Gravida: has been pregnant ii) Primigravida: first pregnancy iii) Multigravida: multiple pregnancies iv) Nulligravida: never been pregnant v) Primipara: first pregnancy or only one child vi) Multipara: has given birth more than two times vii) Nullipara: has never given birth or had a pregnancy beyond the gestational age of an abortion b) Previous pregnancy complications (diabetes, hypertension, preeclampsia) c) Breastfeeding history d) Definitions i) Premature birth <37 weeks ii) Infertility attempting to get pregnant for 1 year 4) Past ObGyn history a) Previous gynecologic disease or procedures i) Procedures (1) Procedure, when, where, and by whome b) STD history c) Immunization history ObGyn Beckman 1

5) Family History 6) Social History a) Toabcco, EtOH, and Drugs b) Intimate partner abuse c) Sexual abuse d) Nutrition and diet e) Caffeine 7) ROS 8) Physical examination a) Breast Examination i) Inspect (1) Hands at the side (2) Hands press down on the hips: visualize pectoralis contraction (3) Arms above the head: observe axillary line (4) At this point one is looking for changes in shape, contourm and symmetry of the breast which may be related to tumors (5) Peau dorange (a) Edema of the lymphatics causing the skin to have a leathery puckered appearance (6) Discoloration/ulceration ii) Discharge (1) Milky white/clear: galactorrhea (usually bilateral) (a) Related to elevated prolactin levels or depress dopamine levels (2) Bloody discharge: inflammation of the breast underlying structures (usually unilateral) (a) Evaluation is necessary to rule out malignancy (3) Pus (a) Tumor or infection related iii) Palpation (1) Should be done with arm at the side and above the head (2) Use a wave like starting out by the tail towards the nipple (3) Press the nipple to try and elicit fluid (a) If fluid is observed collect and culture b) Pelvic Examination i) Positioning (1) Head at 30 degrees and the patient in the lithotomy position ii) Inspection of the external genitalia iii) Palpate (1) Urethra and skene glands (a) Milk the urethra and culture and discharge (2) Palpate the bartholin glands (a) Lateral sides of the vaginal vault iv) Speculum Examination (1) Penderson speculum: nulliparous and post-menopause women (2) Graves speculum: parous women (3) Placing the speculum ObGyn Beckman 2

(a) Non-dominat hands two digits depress the vagina to make an opening then add speculum in the horizontal plane (b) Next, advance the speculum at a 45 degree angle slowly turning the speculum as you advance (c) Apply pressure downward not upward sensitve structures upward (i.e. clitoris and the urethra) (d) Scrapings of the endocervix and exocervix (e) The vaginal walls are examined as the speculum is being withdrawn in the open position for about 1 inch after that close it up and slowly withdraw the speculum as you turn the wrist v) Bimanual Examination (1) Positions (a) Long axis (i) Anteverted, midposition, retroverted (b) Short Axis (i) Anteflexed or retroflexed (c) Note: Retroverted/Retroflexed uterus (i) Difficult to estimate gestational age (ii) Associated with dyspareunia and dysmenorrheal (iii) Obstetric complications of uterine inculcation (d) Posterior cervix: ateverted or midpoistion uterus (e) Anterior cervix: retroverted uterus (2) Adnexa (a) Lateral to the cervix in the vaginal fornix attempt to palpate the adnexa ObGyn Chapter 2: Role in Screening and Preventive Care 1) Introduction a) Primary prevention: eliminate the risk of disease b) Secondary prevention: screening test 2) Immunizations a) DTaP, Hep A, Hep B, meningococcal, influenza, MMR, varicella, pneumococcal, herpes zoster b) HPV vaccination is recommended for females and males 11-26 i) Should attempt to give vaccination before first intercourse, but may be given after 3) Characteristics of Screening Test a) Objective is to catch disease in the aymptomatic state b) The disease should be prevalent in the population and amenable to early intervention c) The disease should be treatable d) Sensitivity: TP/TP+FN e) Specificty: TN/TN+FP 4) Cancer Screening a) Endometrial, vulvar, and vaginal biopsies are not screening test and no screening test for these cancers exist ObGyn Beckman 3

b) Breast Cancer i) Most prevalent cancer amoung women and the second leading COD of cancer related deaths ii) First, assess a patients risk factors for breast cancer using Breast Cancer Risk Assessment Tool iii) Second, for patients at risk two examinations (1) Clinical breast examination (2) Mammography iv) ACOG recommendations (1) Annual breast exam, mammogram every 1-2 years at age 40 v) ACS recommendations (1) Age 20-39: breast exam every 3 years (2) Age 40: annual breast exam and mammogram vi) Very high risk may use MRI for screening vii) NOTE: US and MRI is not needed for average risk patients c) Cervical Cancer i) Begins with cervical intraepithelial neoplasia ii) Screening test: exfoliative cytology (i.e. Pap smear) iii) Annual cytology screening three years after the initiation of intercourse, but not later than 21 iv) Age 30 or older with a history of 3 consecutive negative screening test may have a Pap every 2-3 years IF they have never had CIN2/3, HIV, or DES exposure v) Age 30 or older with negative cytology and DNA sequencing may be screened every three years vi) Total hysterectomy (no Hx of cervical cancer): no longer require Pap vii) Total hysterectomy (Hx of cervical cancer): may be discontinued after 3 consecutive negative vaginal cytology viii) Supracervical hysterectomy still requires Pap d) Colorectal Cancer i) Third leading COD in women from cancer ii) Screening should begin at the age of 50 by colonoscopy every 10 years iii) Other screening test (1) Fecal occult blood and fecal immunohistochemical testing (three samples required) (2) Flexible sigmoidoscopy every five years (may miss R sided lesions which accounts for 65%) (3) Combination of the above e) HIV screening: may use and ELISA and Western Blot f) Chlamydia infections i) Routine screen for younger than 25, high risk women 26 and older. g) Gonorrhea infections i) Routine screen for sexually active adolescents and high risk women 26 and older h) Syphillis i) Serologic test may be negative early on in disease ObGyn Beckman 4

ii) Routine screen for women who are at an increase risk, pregnant women (ASAP and again at delivery), high risk pregnant women at the third trimester iii) Test (1) VDRL, RPR, TP-PA (T. pallidum particle agglutination 5) Metabolic Disorders a) Osteoporosis i) Epidemiology (1) 13-18% age of 50 and older women (2) 37% age of 50 and older women have osteopenia or low bone density ii) Hip and spine fracture leading cause of morbidity and mortality iii) Bone mineral density using dual energy xray absorptimetry (1) T score: standard deviation from the young adult population (a) 1 normal (b) -1 to -2.5 osteopenia (c) -2.5 osteoporosis (2) Z score: standard deviation from the same reference population iv) Recommendations (1) Start at the age of 65 or (2) Postmenopausal women with at least one risk factor v) Prevention (1) Vit.D and calcium supplementation (2) Exercise (3) Step smoking (4) EtOH moderation (5) Fall prevention b) Diabetes Mellitus i) Fasting blood glucose ii) Begin at age 45 and continue every three years (1) NOTE: may want to start screening earlier if risk factors are present (i.e. BMI >25) c) Thyroid Disease i) Measure TSH levels every 5 years after the age of 50 d) Hypertension i) Definition: systolic 140 and diastolic 90 ii) Recommendations (1) Begins at the age of 13 and continues every other year or annually if at high risk e) Lipid Disorders i) Leading COD among both men and women in the US ii) LDL, HDL, and Triglycerides iii) Recommendations (1) Age 45 (no risk factors) Lipid profile and reassess every 5 years (2) With risk factors may begin screening at an earlier age.

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ObGyn Chapter 4: Embryology and Anatomy 1) Embryology Introduction a) Urogenital ridge i) Forms both the gonads and the genitals b) Paramesonephric/mullerian ducts (intermediate mesoderm): ovaries, fallopian tubes, upper portion of the vagina i) Note: the male equivalent are the mesonephric/wolfian ducts: epididymis, ductus deferens, and ejaculatory duct c) Genital swellings: external genitalia d) Male signaling i) Y chromosome -> SRY gene -> testis determining factor e) Female signaling i) WNT4 -> ovary determining gene f) Timeline i) Urogenital ridge: week 5 ii) Gonads: week 7 iii) External genitalia: week 12 (1) Note: the external genitalia are influenced by androgens. An increase in androgens during female development can lead to genitalia anamolies (i.e. congenital adrenal hyperplasia -> most often caused by 21 hydroxylase deficiency) iv) External genitalia can be seen on ultrasound: 15 weeks 2) Germ cell development (female) a) Primordial germ cells migrate from the yolk sac along allantois and the hindgut to the gonadal ridges/primary sex cords b) Failure of this migration resulsts in ovarian agenesis c) The primary sex cords regress and in their place form secondary sex cords/cortical cords d) The cortical cords will further develop to form the primary follicles 3) Germ cell development (male) a) Primary sex cords to not regress and instead form the seminiferous tubules and the rete testis b) The tunica albuginea separates the seminiferous tubules from the surface epithelium c) NOTE: cortical cords do not form in the male 4) Gonad migration a) Females: move with the gubernaculums to the pelvis i) The gubernaculums forms the ovarian and round ligaments b) Males: descend to the scrotum 5) Development of the Genital Ducts (female) a) Regression of the mesonephric ducts (forms the male duct work) b) Formation of the paramesonephric ducts (female duct work) i) Forms the fallopian tubes, uterus, and the upper portion of the vagina c) The paramesonephric ducts contacts the epithelial vaginal plate which will form the lower portion of the vagina ObGyn Beckman 6

6)

7)

8)

9)

d) Upon fusion of the ducts to form the uterus and vagina (upper portion) a fold of peritoneum is taken with them to form the broad ligament Development of the external genitalia a) Urorectal septum separates the cloaca to form the urogential sinus anteriorly and the anorectal canal posteriorly (anus) b) Cranial end of the urogenital sinus forms the genital tubercle (penis/clitoris) and the posterior lateral of the urogenital sinus forms the labioscrotal swellings (labia majora/scrotum) and the urogenital folds (labia minora) Bony Pelvis a) Greater pelvis/false pelvis i) Formed by lumbar vertebrae, the iliac fossae, and the abdominal muscles ii) Contents: abdominal viscera and support a pregnancy b) Lesser pelvis/true pelvis i) Formed by sacrum, coccyx, ischium, and pubis ii) Contents: pelvic viscera c) Clinical correlation i) In obstetrics it is vital to measure the size of the pelvis to determine if a vaginal birth can occur (1) Determined by the measurements of the pelvic outlet, pelvic inlet, and midpelvis (2) Most accurately done by CT, but usually done by pelvic examination using the obstertric conjugate ii) Obstetric conjugate: (1) The smallest diameter the fetus will have to pass through (2) It is estimated by using the diagonal conjugate (3) Diagonal conjugate: is measured from the inferior pubis to the sacral prominence at the levels of the ischial spines (4) Obstetric conjugate = diagonal conjugate + 1.5 to 2.0 cm (must equal 11.0 cm or greater in order to deliver vaginally iii) Interspinous diameter: 10 cm iv) Transverse diameter: 13.5 cm d) Pelvis Shapes (in order of most common to least common) i) Gynecoid: round ii) Anthropoid: oval-long iii) Android: wedge iv) Platypelloid: oval Vulva and Perineum a) Vulva: labia majora, labia minora, mons pubis, and the vestibule b) Labia majora: sebaceous glands, sweat glands, and hair follicles c) Labia minora: sebaceous glands and sweat glands d) Bartholin glands: provide lubrication during intercourse e) Skene glands: paraurethral Vagina a) Children and young women

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i) Vaginal anterior and posterior walls are fused forming an H structure on cross section ii) Underlying rugae connect to the tendinous arch of the pelvic wall b) Age and child birth i) Connection to the pelvic wall weakens causing the structures in the pelvis to be come less stable c) External os i) Nullipara: circle.oval ii) Primapara/multipara: slit d) Blood supply i) Vaginal artery a branch from the hypogastric artery 10)Uterus and Pelvic Support a) Ligaments i) Broad ligament: divisions (1) Mesovarium (2) Mesosalpinx (3) Mesometrium ii) Cardinal ligament: attaches the sides of the uterus inferior to the uterine arteries iii) Suspensory (Infundibulopelvic) ligament: connects the ovaries to the posterior wall of the abdomen and contains the ovrian vessels

b) c) Clinical Correlation i) Uterine artery overlies the ureters Water under the bridge 11)Ovaries a) Blood supply i) Ovarian arteries which are a direct branch from the abdominal aorta ii) Ovarian veins (1) Right ovarian vein drains directly into the IVC ObGyn Beckman 8

(2) Left ovarian vein drains into the left renal vein and then into the IVC 12)Anomalies of the Female Reproductive Systme a) Ovarian dysgenesis: failure of oogonia migration (Turners sydrome) b) Failure of gonad migration (anatomical female genetic male) c) Mullerian agenesis: degeneration of the mullerian ducts d) Failure of mullerian duct fusion i) Bicornate uterus double vagina ii) Bicornate uterus single vagina iii) Bicornate uterus with a rudimentary horn e) Gartner cyst i) Failure of the mesonephric ducts to regress ii) Location: vaginal wall or the broad ligament ObGyn Chapter 5: Maternal-Fetal Physiology 1) Cardiovascular changes a) Anatomic i) Heart is displaced upward, lies horizontally, and the apex is lateral (1) Due to the diaphragmatic elevation b) Physiologic i) Cardiac Output (1) Increase due to an increase in stroke volume (first half of pregnancy) (a) Increase in blood volume which peaks in the 32 week of gestation (b) Decrease in vascular resistance due to progesterone (vasodilation), AC shunting, and uteroplacental circulation, and prostaglandins (2) Increase in maternal HR (second half of pregnancy) (a) Decrease in stroke volume due to decrease venous return from uterine compression of the IVC (i) Overcome venous return by the paravertebral collateral circulation ii) Uterus circulation (1) 2->20% of the CO (2) Circulation to the splanchic bed and the lower extremities is maintained by an increase in CO iii) Blood pressure (1) Initial decrease in diastolic blood pressure followed by an increase to normal values iv) Symptoms (1) Hypotension: dizziness, light headedness, and syncope v) Physical Exam (1) Loud S2 (2) Systolic ejection murmur: due to more blood volume through the heart (3) Distended neck veins and S3 gallop vi) Diagnostic test (1) Monitor bp ObGyn Beckman 9

(2) Elevated bp throughout the pregnancy is abnormal and should be evaluated 2) Respiratory System a) Anatomic i) Elevated diaphragm and widened costovertebral angle b) Physiologic i) Increase in oxygen consumption (1) Gravid uterus (mostly), heart, kidneys, and mammary tissue increase consumption ii) Elevated diaphragm -> decrease in (1) Residual volume (2) Expiratory residual volume (3) Total lung volume iii) Progesterone (1) Increase central sensitivity to CO2 -> increase in tidal volume -> increase in minute ventilation (2) Thus, decrease in pCO2 -> respiratory alkalosis -> compensated by renal increase in excretion of bicarbonate iv) Tidal volume remains the same c) Symptoms i) Dyspnea -> due to physiologic response to low arterial pCO2 d) Diagnostic test i) Arterial blood gas -. Compensated respiratory alkalosis 3) Hematologic a) Anatomic i) Increase in plasma volume, RDW, and coagulation factors ii) Due to the increase in RBC production there is a necessity for increase in iron consumption. (1) Note: fetal Hb levels are maintained regardless of the maternal status (2) Anemic mom requires 60 mg iron supplement per day iii) WBC elevates slightly (1) Note; during labor neutrophils elevate due to stress-associated demargination iv) Clotting factors (1) Increase in the clotting factors as well as a decrease in protein C and S levels -> hypercoagulable state ( impartant in the pueriperium state) b) Functional changes i) Increase in total O2 carrying capacity (1) Increase minute ventilation (2) Increase in Hb concentration ii) Maternal lungs ->left shifted curve (1) Decrease in pCO2 (respiratory alkalosis) (2) Hb high affinity for O2 iii) Placenta -> right shifted curve from high fetal pCO2 (1) Hb low affinity O2 c) Symptoms ObGyn Beckman 10

i) Edema d) Diagnositc test i) CBC (1) Low Hct and Hb (physiologic anemia due to increase in plasma volume) (2) Low Hb (a) 12.5 is within the normal range (b) 11.0 warrants iron therapy and further investigation (3) WBC elevation -> may reach as high as 30,000 (4) Increase in fibrinogen, but no change in PT or PTT 4) Renal System a) Anatomic i) Enlargement of the kidneys and the urinary collecting system ii) Ureters (1) Compression: gravida uterus (2) Dilation: progesterone iii) Bladder (1) Decrease in tone: progesterone (a) Increase in post residual volume (2) Decrease in volume: gravida uterus compression b) Physiologic i) Increase in RPF and GFR ii) Increase in GFR (1) Leads to an increase of filtered solute (a) Glucose: trace increase in urine (b) Sodium: increase in the amount filtered, but is compensated by an increase in reabsorption (c) Protein: NO significant increase in protein loss -> proteinuria remains pathologic iii) Increase in the rennin-angiotensin-aldosterone system (1) Normal pregnancy: no effect (2) HTN disease or HTN or pregnancy: will lead to an increase in bp c) Symptoms i) Increase in frequency due to bladder compression and decrease tone ii) Increase likelihood of pyelonephritis due to increase in post-residulal volume and should be considered in asymptomatic bacteruria iii) Stress urinary incontinence d) Diagnostic test i) UA (1) Increase in BUN and creatinine (2) Increase in blood glucose (3) No change in protein ii) Serum (1) Decrease in BUN and creatinine iii) Imaging -> hydronephrosis 5) Gastrointestinal changes ObGyn Beckman 11

a) Anatomic i) Displacement of the abdominal viscera ii) Increase in size of the portal vein -> increase blood flow b) Physiologic i) Progesterone (1) General smooth muscle relaxation (2) Lower esophageal tone decrease (3) Impaired gallbladder contractility ii) Morning sickness (1) Progesterone iii) Hyperemesis of gravidum (1) Severe N/V (2) Wight loss, ketones, and electrolyte imbalance iv) Dietary cravings, pica, ptyalism (xs saliva) v) Symptoms of GER due to progesterone vi) Constipation (1) Compression of the viscera from the gravidum uterus vii) Intrahepatic cholestasis -> increase in bile acid concentration -> pruritus c) Physical Exam i) Gingival disease (1) Gums become softer (2) Pyogenic granuloma ii) Hemorrhoids (1) Constipation (2) Increase in IVC pressure d) Diagnostic test i) Increase in serum alk. phos. -> placental production ii) Cholesterol levels increase iii) Albumin concentration decreases due to dilution 6) Endocrine System a) Thyroid function i) hCG (1) Thyotropin like substance (2) Increase in maternal T4 secretion ii) Estrogen (1) Increase in hepatic thyroxine binding globulin iii) Overall, no net increase in T4 or T3 levels b) Adrenal Function i) Mostly an increase in overall steroid production 7) Metabolism a) Carbohydrates i) hPL: produced by the placenta decreases insulin sensitivity -> hyperinsulinemia and hyperglycemia (1) Causes a post-pradial hyperglycemia ii) Fetoplacental unit -> drains maternal glucose -> fasting hypoglycemia b) Lipid metabolism ObGyn Beckman 12

i) Early pregnancy increase in lipids, lipoproteins and abetalipoportein ii) Synthesis increases in early pregnancy and then in late pregnancy levels drop due to accelerated starvation from fetal induced hypoglycemia c) Protein metabolism i) Utilization of 1 kg of protein above normal pregnant state 8) Musculoskeletal a) Lumbar lordosis b) Exacerbation of hernia defects c) Relaxation of the pubic smphysis -> progesterone and relaxin d) Increase in maternal PTH to maintain calcium levels due to increase in fetal demand i) No loss of bone density in pregnancy in proper nutrition is maintained 9) Skin a) Spider angiomatas, palmer erythema, striae gravidarum b) Hyperpigmentation -> increase in estrogen, MSH< and hCG i) Linea alba becomes linea nigra ii) Chloasma -> mask of pregnancy iii) Skin nevi increase in size and darken iv) Eccrine and Sebum production increase -> acne 10)Reproductive tract a) leukorrhea of pregnancy -> milk white discharge b) Mucous plug -> endocervix everts into the ectocervix c) Uterine cavity increases in volume and mass 11)Opthalmic a) Blurred vision: increased in thickness of the cornea and decreased intraocular pressure 12)Fetal and Placental physiology a) Placenta i) Function as respiratory and metabolite exchange ii) Gas exchange -> simple diffusion iii) Single most important metabolite for placenta metabolism is GLUCOSE -> facilitated diffusion iv) Amino acid transport -> active transport v) Produces (1) Estrogen, progesterone, hCG, and hPL b) Hemoglobin i) HbF does not bind 2,3-BPG increasing its affinity for oxygen c) Kidney i) Becomes functional in the second trimester ii) Produces dilute, hypotonic urine iii) Primary source of amniotic fluid in the second trimester d) Thyroid gland i) Becomes functional at the end of the first trimester (1) Until then maternal T3 and T4 compensate by crossing the placenta (2) NOTE: maternal TSH cannot cross the placenta e) Immunology of pregnancy ObGyn Beckman 13

i) The fetus blocks itself from the maternal immune system via the placenta ii) IgG is the only immunoglobulin that has the ability to cross the placenta iii) Fetal lymphocyte production begins by 6 weeks gestation ObGyn Chapter 6: Preconception and Antepartum Care 1) Preconception counseling and care a) Vaccinations i) Rubella, varicella, and Hep B (1) Note: rubella and varicella cannot be given to a pregnant women because they are live vaccinations b) Prevention of NTD i) 0.4 mg of folic acid daily while attempting to get pregnant and within the first trimester ii) Prior pregnancy with NTD -> 4 mg c) Test for HIV 2) Diagnosis of pregnancy a) Physical signs of pregnancy i) Missed 1-2 periods in a regular cycling female ii) Morning sickness N/V and breast tenderness b) Physical Exam i) Enlargement and softening of the uterus: 6 weeks or greater -> moved into the lower abdomen by 12 weeks ii) Chadwick sign (1) Genital tract congestion and a bluish discoloration of the vagina iii) Hegar sign (1) Softening of the cervix iv) Hyperpigmentation of the abdominal skin (linae nigra) and straie v) Fetal movement (1) Between 16-18 weeks, but may be as late as 20 weeks vi) Pregnancy test (1) hCG (a) Produced by the syncytiotrophoblast (b) At 4 weeks from the LMP rise sufficiently to test positive for a pregnancy test (c) Structurally similar to LH -> test for the beta-hCG subunit (2) Urine test: Low FP high FN rate (3) Serum: test specifically for the beta subunit of hCG vii) Ultra sound (1) Discriminatory zone (a) The beta hCG level at which one can detect a pregnancy by ultra sound 1. (2) 5-6 weeks: gestational sac (transabdominal) 2. (3) 3-4 weeks: detect pregnancy (transvaginal) (2) Beta hCG levels >4000 mIU/mL should be evaluated for fetal heart activity ObGyn Beckman 14

Fetal Heart Activity 1. (1) 18-20 weeks: fetoscope (2) 12 weeks: Doppler device 3) Initial Prenatal Visit a) H and P i) Physical exam (1) Pelvimetry (2) Cervical assessment (3) Fundus size: can be used to determine gestational age b) Labs i) Blood: Type (erythroblastosis fetalis), Anti-Rh (EF), Hb/Hct/MCV (evaluate for iron deficiency anemia) ii) Pap, HIV, VDRL (TORCH) iii) Vaccinations: rubella, varicella, HbsAg iv) UA and Urine culture -> asymptomatic bacteruria v) Indicated genetic testing vi) STD c) Gestational Age i) Is determined from the LMP, not the time of conception ii) Establishes an estimated delivery date iii) Naegeles rule: (1) Date of LMP + 7days 3 months = EDD iv) Normal pregnancy duration last 40+/- 2 weeks v) US (1) Within 1-2 weeks if estimated within the 14-16 week period (a) Crown to rump length (b) Gestational sac diameter (2) After 14-16 weeks the lower uterine segment makes it hard to determine the gestational age (3) NOTE; a retoverted uterus makes US estimation harder 4) Subsequent Antenatal Visits a) Schedule for appointments (normal pregnancy) i) Every 4 weeks until 28 weeks gestation ii) Every 2-3 weeks past 28 weeks and until 36 weeks iii) Every week past 36 weeks b) What to ask? i) Problems: vaginal bleeding, N/V, dysuria, or vaginal discharge ii) After quickening has begun the mom should be asked about fetal movement (inc., dec., or stay the same) c) Assessments i) BP: want to first establish a baseline and the monitor the BP (preeclampsia) (1) Normal: Will initially decrease followed by return to normal by week 20 (may experience light headedness or dizziness) (2) Gestational Hypertension: (a) Systolic >20 mm Hg rise ObGyn Beckman 15

viii)

(b) Diastolic > 15 mm Hg rise ii) Weight (1) Normal BMI (a) 25-35 lb weight gain total (b) Rate of 3-4 lbs per week (2) Obese BMI (a) Decrease in the recommended total weight gain (b) Increase risk for: gestational diabetes, cesarean, and preeclampsia iii) UA for blood glucose and albumin: baseline establishment required iv) Fundal Height measurements (1) until 18-20 weeks uterine size is noted by gestation age (2) 16 to 36 weeks the fundal height (cm) is used to estimate gestational age (a) After 36 weeks the fetus moves into the pelvis and the fundal height is no longer accurate (3) Equal to the length of the fundus to the pubic symphysis v) Fetal HR: normal 110-160 vi) Palpation for presentation (1) Before 34 weeks breech, oblique, transverse, and cephalic presentations are not uncommon (2) Past 34 weeks most common presentation is (a) Cephalic (b) Breech (bottom first) (c) Shoulders (d) Tranverse (3) Leopold maneuvers (a) First maneuver superior palpation (i) May distinguish the breech presentation -> softer, less round, and difficult to outline (b) Second and third maneuver (i) Palpate on each side (c) Fourth maneuver (i) Slight pressure over the pubic symphysis (d) If in the breech position consult patient on turning the fetus to the cephalic presentation to avoid a cesarean section 5) Ultrasound a) Optimal timing for first ultrasound is between 16 - 20 weeks b) Uses i) Confirm IUP, estimate gestational age, confirm cardiac activity, and evaluate multiple gestations and pelvic masses c) Nuchal transparency i) Identifies chromosomal anomalies (i.e. trisomy 21, 18, 13, and Turner syndrome) (1) Confirm Downs syndrome with biochemical markers (triple screen) d) Assess placental and cervical abnormalities ObGyn Beckman 16

i) Placenta abruption ii) With color flow Doppler -> placenta accrete iii) Transvaginal US: placenta previa and shortened cervix (26-30 weeks increase risk of preterm labor) 6) Screening Test a) Trisomy screening i) First trimester: (1) US (NTT), Beta hCG, pregnancy associated plasma protein-A (PAPP-A) ii) Second trimester (1) Triple screen (serum) (a) AFP, hCG, and estriol (2) Quad scress (serum) (a) AFP, hCG, estriol, and inhibin iii) Integrated first and second trimester screening (1) Beta hCG, pregnancy associated plasma protein-A (PAPP-A) (2) Quad scress (serum) (3) +/- US (NTD) iv) Gestational diabetes (1) Glucose challenge test (2) Glucose tolerance test v) GBS (1) 32 and 36 weeks 7) Fetal Assessment a) Fetal Growth i) Fundal height measurement (16- 36 weeks) (1) Fundal height >> expected -> large for gestational age differential (a) Inaccurate estimation for the gestational age (b) macrosomia (c) multiple pregnancies (d) hydatid form mole (e) polyhydroamnios (2) Fundal height << expected -> small for gestational age differential (a) Oligohydroamnios (b) Hydatid form mole (c) Intrauterine growth restriction (d) Inaccurate estimation for the gestational age ii) US (1) Most useful weeks 14-16 b) Fetal Well-Being i) Fetal activity (1) Kick counts (2) Common indirect measure of fetal well-being ii) Nonstress test (1) Design: measurement of fetal heart rate in a 20 minute window (2) Reactive NST: 2 or more fetal heart accelerations +/- fetal movement (3) Nonreactive NST: no fetal heart accelerations in a 40 minute window ObGyn Beckman 17

iii) Contraction Stress test (1) Design: tocodynamometer(measure contractions) and fetal heart rate transducer are placed on the abdomen and a contraction is elicited using nipple stimulation or oxytocin (2) Physiologic principle (a) With contraction the fetal circulation is compromised and the fetus should be able to compensate to maintain for the decrease in blood flow (3) Negative: no change in fetal heart rate with contraction -> fetus is good health (4) Positive: decelerations of the fetal HR (a) Must be confirmed with repeatability iv) Biophysical Profile (1) Similar to an APGAR score: five categories rank 0-2 (2) Categories (a) NST, fetal breathing, fetal movement, fetal tone (flexed extremities), and quantification of amniotic fluid (3) Score of 8-10 is reassuring (4) Modified BPP (a) NST and amniotic fluid quantification (i) Oligohydroamnios -> decrease support for the umbilical core > reducing blood flow to the fetus v) Doppler US of the umbilical artery (1) Design: measure systolic and diastolic pressure ration (a) TPR increases diastolic blood flow decrease -> increase in the systolic/diastolic ratio -> placenta insufficiency (b) Reversed-End flow -> intrauterine growth restriction secondary to uteroplacental insufficiency vi) Fetal Maturity (1) Focuses mostly on the development of the fetal respiratory system (2) Measure in various ways (a) Lecithin/Sphingomyelin ratio > 2.0 is associated with fetal lung maturity (b) Phosphatidylglyceroal -> marker of complete pulmonary maturation, present at 35 weeks 8) Antepartum Patient Education a) Employment i) A pregnant women should be able to continue work all the way up until labor with a few restrictions ii) A period of 4-6 weeks after the delivery should be taken before returning to work b) Exercise i) 30 minutes of moderate exercise per day ii) Supine exercises should be avoided iii) Hyperthermia may be teratogenic, so hot tubs and sauna should be avoided ObGyn Beckman 18

(1) Saunas no more than 15 minutes (2) Hot tubs no more than 10 minutes 9) Nutrition and Weight Gain a) RDA of iron in the pregnant female 27 mg iron b) Weight gain i) Maternal 16.7 lbs ii) Fetal 10.6 lbs iii) Total: 27.3 lbs 10)Sexual Activity a) Not restricted except under cases of high risk pregnancy b) Consideration should be taken for more comfortable positions 11)Travel a) Up to 36 weeks b) Air travel is not recommended for women with medical or obstetric complications i) HTN, uncontrolled diabetes, sickle cell disease c) Seat belt should be worn between protuberant abdomen and the pelvis 12)Medications a) Page 71-72, tables 6.5-6.6 13)Methyl Hg a) Found in contaminated fish (i.e. albacore tuna) b) Pregnant women are instructed not to eat more than 6 mg of albacore tuna/week and no more than 12 mg of fish/week 14)Herbal Remedies to Avoid a) Echinacea, Black Cohosh (estrogen analog), Garlic and willow bark (anticoagulants), Ginkgo (inhibits MAO), Licorice, Valerian, Ginseng (inhibits MAO), Blue Cohosh and pennyroyal (stimulates uterine musculature) 15)Alcohol a) Greatest sensitivity is during the first trimester b) Fetal Alcohol Syndrome i) Growth restriction ii) Facial abnormalities (1) Smooth philtrum and thin upper lip (2) Shortened palpebral fissures (3) Midfacial hypoplasia iii) CNS dysfunction (1) Microcephaly, mental retardation, and behavioral problems iv) 8 or more drinks daily 16)Tobacco use a) Intrauterine growth restriction, low birth weight, fetal mortality 17)Substance abuse a) Fetus born to mothers who have taken opiates during pregnancy may develop withdraw b) Babies are exposed in utero through the placenta and through breast milk 18)Common Symptoms a) Headache -> acetominophen ObGyn Beckman 19

b) Edema -> common, but if extensive evaluate bp c) Nausea and vomiting -> i) Change diet ii) Vit. B6 iii) Vit. B6 and doxylamine iv) Antihistamine H1 blockers v) Phenothiazine d) Heartburn -> smaller, more bland meals e) Constipation -> i) Fiber ii) Docusate (stool softener) iii) Psyllium hydrophilic mucilloid f) Leg Cramps -> Ca2+, K+, rest ObGyn Chapter 7: Assessment of Genetic Disorders in ObGyn 1) Replication Errors a) Missense mutations: substitue of AA b) Nonsense: premature stop codons are inserted into a sequence c) Deletions d) Insertions 2) Meiosis a) Prophase I -> crossing over (pachytene step) b) Anaphase 1 -> most error prone stage in meiosis; independent assortment c) Non-disjunction: common cause of chromosome abnormality 3) Abnormalities in chromsome number a) Herteroploidy: alterations in the number of chromosomes i) Euploidy: whole set of chromosome is duplicated 2n (46) -> 3n (69) ii) Aneuploidy: diploid number 46 is altered -> trisomies b) Page 80, Table 7.1 i) Trisomy 16 -> fetal death in utero 4) Abnormalities in chromosome structure a) Deletion: loss of chromosome segment resulting in imbalance (DMD) b) Insertion: segment from one chromosome is inserted in another (Hemophila A) c) Inversion: a single chromosome has two breaks and then flipped insertion (inv 9) d) Robertsoninan translocation: two acrocentric chromosomes break forming one large chromosome (long arms) and a short chromosome (short arms) i) Phenotypically normal with abnormal gametes ii) Acrocentric chromosomes -> 13, 14, 15, 21, and 22 e) Recipriocal translocation: breakage of nonhomologous chromosomes and recombination i) Balanced reciprocal translocations have phenotypically normal, with abnormal gametes 5) Phenotypic Expression ObGyn Beckman 20

a) Variable expressivity -> degree of the disease varies from person to person b) Penetrance -> likelihood a person carrying a mutated gene will express it c) Anticipation -> triplet repeat diseases; i.e. Huntington disease 6) Risk factors for genetic disorders a) Advance maternal age 35 yo increase risk of Downs syndrome b) Advance paternal age -> increase risk of X linked recessive and autosomal dominant diseases c) Previous pregnancy of a trisomy child has an increase risk of having another trisomy child (mostly relating to somatic trisomy) d) History of early pregnancy lost -> 50% are due to chromosome abnormalities 7) Prenatal Screening a) Screening test: is the fetus at risk for a disease b) Diagnostic test: does the at risk fetus have the disease c) First trimester screening: i) hCG > 1.98 elevation indicates euploidy ii) PAPP-A -> decrease indicates Down syndrome iii) US -> nuchal transperancy -> chromosomal abnormalities iv) NOTE: CVS chorionic villous sampling to test for genetic abnormalities may be the next step if any of these test return positive for disease d) Second trimester screening: i) Triple Screen (1) Downs Sydrome (a) AFP, hCG, Estriol (2) Edwards Syndrome (a) AFP, hCG, Estriol ii) Quadruple Screen (1) Downs Syndrome (a) Triple screen results and inhibin A 8) Ultrasound Screening a) Second trimester i) Identify cardiac defects and subtle soft tissue defects (increase risk of Down syndrome) 9) Screening for NTD a) Elevated maternal serum AFP b) NTD is the second most common congenital abnormality (number one is cardiac abnormality) c) Risk is reduced by folic acid supplementation 10)Integrated screening a) US (for NT), PAPP-A (downs syndrome), QUAD screen b) Advantage: lower false positive rate c) Disadvantge: have to wait until further in the pregnancy to run the integrated test and miss out on CVS 11)Carrier Testing a) Ashkenazi Jews i) Tay-Sachs, Canavan, CF, and familial dysautonomia 12)Fetal diagnostic Procedures ObGyn Beckman 21

a) Amniocentesis i) Should wait until 14 weeks gestation to avoid loss of pregnancy ii) The safety of amniocentesis match with its diagnostic power indicates a strong diagnostic tool b) Chorionic Villous Sampling (CVS) i) Should wait until 10 weeks gestation ii) Rate of pregnancy loss similar to amniocentesis iii) First trimester test c) Percutaneous Umbilical Blood Sampling i) 20 weeks gestation ii) CBC of the fetus iii) karyotype of the fetus iv) second step test after chromosomal mosaicism established via amniocentesis/CVS 13)Tests a) Karyotype b) FISH: 13, 18, 21, X, and Y chromosomes may be analyzed c) Spectral Karyotyping (SKY): all chromosomes can be analyzed d) Comparative Genomic Hybridization: identifies submicroscopic chromosomal deletions and duplications 14)Gynecologic Genetic Screening a) BRCA1 and BRCA2 -> hereditary forms of breast and ovarian cancer i) BRCA -> increase incidence in Ashkenazi Jews ii) HNPCC A (Lynch I Syndrome): increase risk of colon cancer (1) Also linked to endometrial, uteral, and renal cancer iii) HNPCC B (Lynch II Syndrome): (1) Autosomal dominant (2) Increases risk of all type I cancers as well as ovarian, gastric, and pancreatic (3) NOTE: HNPCC AD -> defect in DNA mismatch repair ObGyn Chapter 8: Intrapartum Care 1) Maternal Changes Before the Onset of Labor a) Uterine contractions i) Braxton Hicks (false) contractions (1) Not associated with uterine contractions (2) Shorter in duration and less intense (3) NOT associated with cervical change ii) True contractions (1) Felt over the uterine fundus and radiate to the lower back (2) Associated with cervical change iii) Lightening: movement of the fetal head into the pelvis (1) Increase in uterine frequency due to increase bladder compression (2) Breathing more easily due to descent into the pelvis iv) Bloody show ->Blood tinged mucus ObGyn Beckman 22

(1) Thinning of the cervix (effacement) and loosening of the mucus plug 2) Evaluation of labor a) When to call for labor? i) Contractions occurring every 5 minutes for at least one hour ii) Bloody show iii) Significant vaginal bleeding iv) Decrease in fetal movement b) Lepold maneuvers i) Four palpations of the fetus through the abdominal wall that helps determine fetal lie, presentation, and position ii) Lie: is the relation of the long axis of the fetus and the maternal long axis iii) Presentation: is the portion of the fetus that is lowest in the birth canal (1) Most common cephalic presentation head is positioned against the chest such that the occiput or vertex presents iv) Position: is the relation of the fetal presenting part to right or left side of the maternal pelvis c) Effactment: shortening of the cervical canal to a more circular orifice with paper thin edges d) Cervical position and changes of labor i) An anterior position cervix is more likely to undergo ripening than a posterior cervix e) Fetal station i) Level of the presenting fetal part in relation to the ischial spines ii) Presenting at the level of the ischial spines is deemed 0 (1) Distance from the pelvic inlet/outlet are divided into fifths

iii) iv) Featl station zero is an important landmark b/c the fetus has negotiated the pelvic inlet 3) Stages of Labor a) Stage 1: (Latent) begging of uterine contractions and cervical ripening; cervical dilation < 4cm (upper limit for latent phase is 14 hours). (Active) Cervical dilation from 4-10 cm ObGyn Beckman 23

b) Stage 2: Delivery of the fetus c) Stage 3: Delivery of the placenta (should occur within 30 minutes of the fetal delivery) d) Stage 4: time after the delivery of the placenta; approximately 2 hours 4) Mechanisms of Labor (cardinal movements of labor) a) Changes of the fetal position as it moves through the uterus b) Accomplished by forceful contractions of the uterus c) Engagement: descent of the head below the pelvic inlet -> a strong indicator that the fetus can make it through the pelvis d) Flexion: fetal head flexes e) Descent: required for successful completion of the passage through the birth canal; occurs during the active phase of the first stage and second stage of labor f) Internal rotation: the head moves to fit through the pelvis -> usually transverse to anterior/posterior g) Extension: after reaching the itroitus the head flexes to accommodate the birth canal h) External rotation: the head rotates to face forward i) Expulsion

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j) 5) Normal Labor and Delivery a) Position: dorsal lithotomy for vaginal and c-section births b) Fluid management and oral intake i) sips and chips concern over aspiration ii) IV fluids: (1) normal saline (normal saline may be used, if you desire increase oncotic pressure) (2) D5 normal saline (3) AVOID lactated ringers b/c of metabolic acidosis incurred by lactate administration c) Evaluation of Fetal Well-Being i) Fetal Heart Rate (1) Stethoscope, hand-held Doppler, or electronic fetal monitoring (one lead EKG) (2) Tocodynamometer is used for monitoring contractions

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d) Control of Pain i) Visceral pain: T10-12 and L1 ii) Somatic pain: S2-4 -> pudendal nerve iii) Analgesia methods (1) Epidural block (2) Spinal anesthetic (3) Combined epidural block and spinal anesthetic (a) Decrease likelihood of postdural puncture headache (4) Local block of the pudendal nerve (a) Episiotomy or perinal laceration repair (b) May result in fetal bradycardia (5) General anesthesia: reserved for c-sections e) Management of labor i) First stage (1) Vaginal examination (a) Cervical dilation, effacement, station, position of the presenting part, and rupture of membranes (2) Rupture of membranes (a) Place intrauterine pressure catheter/ fetal scalp monitor (b) Presence or absence of meconium (c) Risk: infection if the labor is prolonged, umbilical cord prolapse if engagement has not occurred ii) Second stage (1) Fetal head begins to mold and may develop caput succedaneum (a) Note may lead to overestimate of station (b) Should last between 2-3 hours (2) If descent does not occur an episiotomy should be considered (3) Fetal head crowns and extends with external rotation (a) Modified Ritgen maneuver may be used to deliver the chin (4) Delivery of the shoulders (a) Downward traction to deliver the anterior shoulders (b) Upward traction to deliver the posterior shoulders iii) Third stage (1) Delivery of the placenta (a) The uterus becomes globular, gush of blood, and the cord lengthend -> indicating separation of the placenta (2) Uterine inversion -> early traction on the cord before separation -> hemorrhage is imminent (3) Placenta passage >30 minutes may be removed manually (4) After the placenta has been delivered the uterus should be palpated to assure contraction to reduce size (a) If the uterus does not contract (i) Uterine massage (ii) Oxytocin, methergine, or prostaglandins (5) Evaluate birth canal for obstetric lacerations

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(a) First degree: vagina mucosa/perineal skin; no underlying structures (b) Second degree: underlying subq tissue; no rectal sphincter or mucosa (c) Third degree: extends to the rectal sphincter, not to the rectal mucosa (d) Fourth degree: extends to the rectal mucosa iv) Fourth Stage (1) First hour after delivery the risk of post-partum complications is at its greatest 6) Labor Induction a) Oxytocin i) Low dose and frequency (1) Lower incidence of hyperstimulation, but longer period to delivery ii) High dose and frequency (1) Faster to delivery, but higher incidence of hyperstimulation b) Cervical ripening i) Must occur before contraction induction (1) Misoprostol (PGE2 analog) vaginal (2) PGE2: vaginal/intracervical (3) Should not be administered together in cases of previous cesarean or uterine surgery (4) Mechanical dilation with laminaria (a) Complications: failure to dilate the cervix, laceration, rupture of membranes, and infection (5) Sweeping the amniotic membrane 7) Cesarean Delivery a) Indications for cesarean section i) Placenta previa, abruptio placentae, prolapse of the umbilical cord ii) Maternal request of C-section should be avoided because it incrases the risk of (1) Placenta previa, placenta accreta, and gravid hysterectomy iii) Vaginal birth after C section (1) Incision through thin segment of the lower uterus -> good to go (2) Incision through the thick muscular segment -> increase risk of uterine rupture -> no go ObGyn Chapter 9: Abnormal Labor and Intrapartum Fetal Surveillance 1) Abnormal Labor (labor dystocia) a) Leading indication for primary C section b) Failure to progress -. Lack of cervical dilation or movement of the head into the maternal pelvis 2) Factors that contribute to a normal pregnancy (three ps) a) Power (uterine contractions), passenger (position, size, and presentation) passage (pelvis/soft tissue) ObGyn Beckman 27

b) Power (uterine contractions) i) Measure: palapation, tocodynamometry (strap arounf the abdomen), or intrauterine pressue cathers ((IUPC) ii) Tocodynamometry -> measures uterine frequency and duration iii) IUPC -> measures uterine frequency, duration, and power (mmHg) (1) Useful in maternal obesity iv) Power (1) 25 mmHg is required for cervical dilation/fetal descent (2) 50-60 mmHg is ideal v) Frequency (1) Three contractions within a 10 minute window is ideal. (2) A rest interval should occur to allow uteroplacental flow to return vi) Monevidea unit (1) 10 minute additive measure of uterine contractions (2) Normal > 200 mmHg c) Passenger (Fetal factors associated with dystocia) i) Head position (1) Flexed (ideal; chin flexed on fetal chest), brow, face, extension, mentum anterior (chin towards Moms abdomen) (a) Bow presentation: convert to vertx or face presentation -> if persistent CS (b) Face presentation: CS (c) Mentum anerior presentation: if converts to a flexed position instead of an extension position may be able to deliver vaginally ii) Persistent occipitoposterior position (1) Longer labor -> 1 hour multiparous; 2 hour nulliparous iii) Compond presentation (1) One or more limb prolapse alongside the presenting part (a) Extremity usually retracts (b) If not, CS required -> associated with prolapse cord d) Passage (Maternal factors) i) Cephalopelvic disproportion (1) The fetal head > maternal pelvis (2) Maternal pelvis can be measured using radiograph < CT < clinical pelvimetry (3) The best way to tell is progression of the descent of the fetus ii) Soft tisse (1) Cervix size, tumors, distended bladder, and uterin fibroids e) Risk i) Chorioamnionitis: prolong rupture of membranes ii) CS -> maternal soft tissue injury, lower gential tract and fetal trauma 3) Diagnosis and Management of Abnormal Labor a) Graphic documentation of progression of the labor b) Protraction disorders -> active and latent phase disorders c) Arrest disorders -> active phase d) Ranges from observation CS ObGyn Beckman 28

e) Protraction i) Latent phase (1) Nulliparous > 20 hours (2) Multiparous > 14 hours ii) First stage (1) Nuliiparous cervical dilation rate < 1cm/hr (2) Multiparous cervical dilation rate <1.2-1.5cm/hr iii) Second stage (1) With regional anesthesia > 3hours (2) No regional anesthesia >2 hours/ fetus descends at a rate less than 1 cm/hr f) Arrest i) First Stage (1) No cervical dilation for more than 2 hours ii) Second Stage (1) No descent after 1 hour of pushing 4) First-Stage Disorders a) Prolong latent phase i) Often due to false contractions ii) Workup: observation and sedation iii) Often indicates false labor, active labor, or prolong active phase b) Prolong active phase i) Augmentation: stimulation of uterine contractions when spontaneous contractions have failed to dilate the cervix/descent of the fetus (1) amniotomy, oxytocin, continuous support (2) Considered when contractions <3 in 10 minutes or not above 25 mmHg of power (the minimum amount to aid in fetal descent) (3) Amniotomy (a) Advantages: may enhance the progress of the active phase and negate the need for oxytocin (b) Disadvantages: fetal heart rate deceleration du to cord compression and chrioamnionitis 5) Second Stage Disorders a) The length of the second stage is not initseld an absolute or even a string indication for operative or CS delivery i) As long as there is good FHR and cephalopelvic disotortion has been ruled out then the second stage can continue ii) What to do? (1) Changing labor position (2) Waiting for the epidural to wear off to regain tone of the pelvic floor muscles (3) Fetal malpresentation -> physcian manipulation 6) Operative Delivery a) Vaginal operative delivery -> forceps or vacuum i) Should only be done by someone has been skilled in it ii) Increase risk of intracranial hemorrhage ObGyn Beckman 29

iii) Outlet Operative Vaginal delivery (1) Scalp is visible at the introitus without separating the labia (2) Fetal skull has reached the pelvic floor (3) Sagittal suture (AP), or R/L occiput (AP) (4) Fetal head is at or on the perineum (5) Rotation does not exceed 45 degrees iv) Low Operative Vaginal Delivery (1) At station 2+ v) Midpelvis operative vaginal delivery (1) Above station 2+ b) Indications and Contraindications i) Vacuum is contraindicated in gestation less than 34 weeks because of risk of intracranial hemorrhage ii) Vacuum is contraindicated in cases of bone demineralization (osteogenesis imperfectica) or bleeding disorder c) Forceps i) Used mostly to mold the head into the proper position ii) Maternal complications: perineal trauma, hematoma, and pelvic floor injury iii) Fetal complications: musculoskeletal injury, corneal abrasion, and shoulder dystocia d) Vacuum extraction i) Less maternal trauma than forceps, but carries with it more fetal risk ii) Neonatal risk: cephalohematoma, intracranial hemorrhage, subgleal hematomas, retinal hemorrhage, and hyperbilirubinemia 7) Breech Presentation a) Associated with i) Prematurity, pregnancy, polyhydroamnios, hydrocephaly, and ancephaly ii) Types of breech presentations (1) Frank -> heads towards the feet (2) Complete -> legs folded Indian style (3) Footling -> the foot is the first structure presented iii) Complications -> cord prolaps b) External cephalic presentation: i) Applying pressure to the Mothers abdomen in order to achieve a vertx presentation prior to labor ii) Works best with gestational age of 36 wks (b/c if the fetus should have flipped by now if it was going to) iii) Selection criteria (1) Normal FHR (2) Adequate amniotic fluid (3) No uterine operative scars iv) Complications (1) Premature rupture of membranes, placental abruption, cord accident, and uterine rupture ObGyn Beckman 30

(2) More successful in parous women and with multiparous women it is advised to add a tocolytic agent before attempting ECV c) Preferred method of breech presentation is a CS i) NOTE: only frank and complete breech can be born vaginally 8) Shoulder dystocia a) Associated with multiparity, post-term gestation, previous Hx of macrosomia/shoulder dystocia b) Turtle sign: head may retract against the maternal perineum c) Delivery i) McRoberts maneuver -> suprapubic pressure to dislodge shoulder (Mom brings legs to the chest (1) NOTE; fundal pressure may worsen dystocia ii) Direct fetal manipulation or delivery of the posterior arm first iii) Zavanelli Maneuver -> fetal head is flexed an reinserted (regain umbilical blood flow) for CS iv) Fracture of the fetal clavicle d) Associated with brachial plexus injury 9) Intrapartum Fetal Surveillance a) Recognize fetal oxygenation status that could result in serious complications b) NOTE; neurological disorders are in fact attributable to other causes not associated with labor (birth asphyxia) 10)Pathophysiology a) Uteroplacental insufficiency i) Signs: fetal heart deceleration (1) Shunting of blood to the fetal brain, heart and adrenals (2) Anaerobic glycolysis -> metabolic acidosis -> lactic academia -> toxic to the brain and myocardium b) Neonatal encephalopathy i) CP: difficulty breathing, hypotonic, decrease levels of consciousness, and +/- seizures ii) Has been demonstrated that 70% of cases are associated with factors that occurred before labor c) Hypoxic- ischemic encephalopathy i) Subtype of neonatal encephalopathy ii) Cerebral palsy -> spastic quadriplegia is associated with HIE 11)Intrapartum Fetal Heart Monitoring a) Measure: i) Internal electonic fetal monitoring (EFM) -> electrode to the scalp/presenting part of the fetus ii) External fetal monitoring -> Doppler b) Detect signs of fetal jeopardy c) Fetal heart rate patterns: i) Normal = 120-160 bpm ii) Fetal bradycardia <120 (1) 100-120 bpm can be tolerated if there is variability (2) 80-100 bpm not good ObGyn Beckman 31

iii) Fetal tachycardia >160 bpm (1) Most common cause is chorioamnionitis (2) 160-200 with fetal variability is usually well tolerates iv) Fetal Heart Variability (1) Graded (a) Minimal 5 bpm (b) Moderate 6 M 25 bpm (c) Marked 25 bpm (2) Moderate variability is an assuring sign and regardless of other FHR patterns the fetus is not experiencing cerebral tissue hypoxia (3) Decrease variability is associate with pathology v) Periodic FHR changes (1) Associated with contractions and are classified by acceleration or deceleration (2) Accelerations (a) Reassuring fetal status and absence of hypoxia or academia (b) Stimulate via fetal scalp stimulation or vibroacoustic stimulation (3) Decelerations (a) Gradual -> onset to nadir 30 seconds (b) Abrupt -> onset to nadir <30 seconds (4) Early: (a) Mirror image of the fetal contraction (b) Due to vagal stimulation and Ach release at SA node to deceleration (c) Physiological no concern (5) Late Decelerations (a) Onset, nadir and resolution occur after the onset of the contraction (b) Most common cause is uteroplacental insufficiency (6) Variable (a) Abrupt fetal deceleration (b) May start before, during, or after a contraction (c) Indicative of cord compression or oligohydroamnios (d) Most common FHR deceleration (e) Tx: (i) Changing of the position of the Mom to relieve cord compression (ii) Amnioinfusion to relieve cord compression from oligohydroamnios (7) Ancillary test (a) To confirm positive EFM (b) Fetal stimulation -> elicit variability or acceleration (i) Fetal scalp stimulation (ii) Allis clamp stimulation (iii) Vibroacoustic stimulation (iv) Digital scalp examination (v) Acceleration after stimulation can effectively rule out fetal ObGyn Beckman 32

acidosis 1. NOTE: if FHR does not accelerate then may try fetal blood pH and lactate levels through fetal scalp sampling (not commonly used) (8) Nonreassuring FHR pattern diagnosis and management (a) Diagnosis of impending hypoxia (i) Recurrent severe variable decelerations or sustained bradycardia without variability (ii) Management: 1. change position 2. administer oxygen for maternal hypotension 3. discontinue oxytocin 4. administer tocolytic 5. if uterine hyperstimulated -> beta adrenergic agaonist 6. if labor is progressing quickly deliver vaginally if not CS 12)Meconium a) Composition: amniotic fluid, lanugo, bile, fetal skin, and intestinal cells b) Passage of meconium in utero is a sign of fetal stress c) Meconium aspiration syndrome: i) Complications: pneumonia, pneumothroax, and pulmonary artery HTN ii) Tx: vigorous suctioning and if in severe respiratory distress intubate and sunction ObGyn Chapter 10: Immediate Care of the Newborn 1) Initial care of the newborn a) Delivery room assessment i) Four characteristics to define if a newborn requires NO additional resuscitation (1) Full term (2) Clear amniotic fluid (3) Spontaneous breathing and crying (4) Good muscle tone ii) Ballard scoring system: assess neuromuscular and physical maturity iii) APGAR scoring system (1) Five signs scored as 0,1, or 2 (2) Assigned at 1 (to identify infants in respiratory distress)and 5 minutes(to determine to effectiveness of resuscitation) (<7 at 5 minutes scored at every 5 minutes until 20 minutes therafter) (3) 7-10: requires no active resuscitation (4) 4-7: mild to moderately respiratory depression (5) Less than 4: requires immediate resuscitation b) Routine Care i) Dry infant and keep warm (1) Skin to skin contact with mother begins bonding and makes breastfeeding after easier ii) Premature infant has trouble regulating body temperature -> add ObGyn Beckman 33

warming pads and hated towels iii) Umbilical cord (1) Clamp, cut, antibiotic (2) White/blue -> blackened and dry -> sloughs off iv) Viral signs measured every 30 minutes v) Breast fed term infants should be left with their mothers to facilitate bonding and placed at the breast 2) Transitional Care a) Changes that are concerning and other care i) Temperature instability, change in acvitity, refusal to eat, change in skin color, abnormal cardiac or respiratory activity, abdominal distention, delayed stools, delayed voiding ii) Antibiotics to the eyes (erythromycin or tetracycline) -> prevent gonococcal aphthalmia neonatorum iii) Vitamin K iv) No passage of stool is indicative of an imperforate anus v) Stool color change from dark green to yellow and seedy with milk consumption b) Circumcision i) First two days of life and is an elective procedure c) Jaundince i) Most often benign, but needs to be evaluated for severe hyperbilirubinemia which can lead to kernicterus (bilirubin mg/dL) ii) Breastfeeding jaundice: decrease in intake of milk leads to decrease excretion of bilirubin iii) Breast milk jaundice: contents of the breast milk leading to jaundice iv) Elevation of direct bilirubin warrants further investigation and possible phototherapy/exchange transfusion 3) Initial Care of the Ill Newborn a) Neonatal resuscitation i) After intubation and no response try epinephrine ii) If epinephrine does not work consider hypovolemic shock and administer fluids iii) Stimulating the soles of the feet by rubbing or flicking to stimulate the infant to breath iv) Maternal narcotic administration (1) naloxone is contraindicated because it will cause an acute withdrawal symptom b) Umbilical cord blood gases i) Metabolic state analysis is through the UMBILICAL ARTERY blood gas (1) In order to circumvent this problem a paired sample of both umbilical vain and artery should be obtained ii) Acidemia umbilical artery pH < 7.20 iii) Fetal asphyxia: hypoxemia, hypercapnia, and metabolic acidosis (base deficit 12) (1) Base deficit deterimens metabolic acidosis severity ObGyn Beckman 34

c) Umbilical cord banking i) Contains life saving hematopoietic stem cells 4) Newborn Screening a) Heel stick for metabolic, Hbopathies, hearing loss, and CF ObGyn Chapter 11: Postpartum Care 1) Physiology of Peurperium (6-8 week period after birth during which the body returns to the non-pregnant state) a) Involution of the uterus i) Immediate post labor the fundus can be felt btw. the pubic symphysis and the umbilicus ii) 2 weeks: uterus returns to the pelvis iii) 6 weeks: at normal size iv) Return to normal size is caused by autolysis of cellular protein -> decrease in the size of the cell not the quantity b) Lochia i) Sloughing occurs because of uterine contraction and loss of blood supply ( similar to the menses cycle) ii) Decidua layer differentiates and is sloughed off (1) Lochia is the sloughing of the decidua and last usually up to 2-3 days , but may last weeks iii) Basal layer becomes the source of the new endometrium -> should be restored by the end of the third week. iv) Classifications (1) Lochia rubra: similar to a period flow (2) Lochia serosa: a lighter discharge with less blood (3) Lochia alba: whitish discharge which may persist v) Women who breast feed resolve lochia faster c) Cervix and Vagina i) Within several hours the cervix has reformed and by 1 week can only fit a finger ii) Shape of the os changes from a circle to a fish mouth in nulliparous women iii) Breastfeeding vaginal mucosa reflects a hypoestrogenic state d) Return of Ovarian function i) Breastfeeding elevated prolactin decreases estrogen levels inhibiting ovulation e) Abdominal wall i) Lightening of the striae gravidum ii) Diastasis recti resolve over time f) Cardiovascular system i) 5 kg weight loss after delivery due to diuresis and loss of extravascular fluid ii) Elevated CO and HR should decrease within a few hours after birth (elevations may contribute to maternal decompensation in patients with ObGyn Beckman 35

heart disease g) Hematopoietic System i) Leukocytosis persist for few days after labor and minimizing the usefulness to determine post-partum infection via labs h) Renal System i) GFR returns to normal levels within a few weeks, but should be considered when dosing medications ii) Renal pelvis and ureter dilation regresses iii) Edema of the urethra may result in transitory urinary retention iv) Transitory stress related urinary incontinence 2) Management of the Immediate Postpartum Period a) Hospital stay i) Vaginal 48 hours ii) CS 96 hours (1) Note excluding the day of the delivery b) Maternal Infant bonding encourage (Mom needs to spend as much time with baby as possible) c) Postpartum complications i) Postpartum hemorrhage (1) Evaulation: (a) Tonic uterine fundus, observe blood loss on pad, BP, and HR observed closely for several hours (2) Days 8 and 14 post partum may have an increase in lochia due to separation of the placental eschar (3) Delayed post partum hemorrhage (a) Tx: suctioning and oxytocin drugs (b) 1/3 of cases have retained placental tissue d) Analgesia i) Local, epidural, or spinal ii) Beware of opiates because the cause respiratory depression and decrease in intestinal mobility e) Ambulation i) Encouraged ASAP to avoid DVT, PE, and urinary retention f) Breast Care i) Breast Engorgement: not breastfeeding women (1) Abates over time and women should be counseled to not stimulate the breast (2) Tx: ice packs and analgesia ii) Galactocele: blocked mammary duct iii) Mastitis (1) Sudden onset fever, localize pain and swelling (2) Micro: S. aureus, GABHS, (beta) H.influenza, E. coli (3) Continue breast feeding and appropriate antibiotics iv) Breast abscess (1) Mastitis + fluctuant mass (2) Antibiotic therapy +/- surgical drainage ObGyn Beckman 36

g) Immunizations i) Rubella ii) TDaP (at least 2 years post vaccine of tetanus-diptheria shot iii) Rh- mom; Rh+ child -> anti-D Ig iv) Infant: HepB h) Bowel Bladder Function i) Mothers may not have a bowel movement for a few days due to lack of intake/fourth degreee episiotomy ii) Hemorrhoids should be monitored and involute within 6 months (1) Greater than 6 months consider surgical procedure iii) Transient urinary retention (1) Due to edema of the urethra (2) May have to place a catheter i) Care of the perineum i) Oral analgesics, ice packs, or warn sitz baths for discomfort ii) Dehisence (rupture of the incision) j) Contraception i) Irregardless of breast feeding one may start combination pills (may reduce lactation) or progesterone only pills ii) Postpartum sterilization -> minilaparotomy performed after CS or vaginal delivery (1) Note if complications arise than minlap cannot be done at the time of the birth k) Sexual Activity i) Minor risk of hemorrhage and infection at 2 weeks ii) Breastfeeding Moms may have pain due to low lubrication from hypoestrogen stater (1) Add lubrication or estrogen vaginal suppositiories l) Weight loss i) To maintain breastfeeding should be at a rate of 2lbs/month m) Lactation and breastfeeding i) Recommended that the infant is exclusively breastfed for 6 months and then continued to be breastfed as mutually desired ii) Contraindications (1) HIV (vertical transmission) (2) Chemotherapy or radiation (3) Tb requires the mother not be in close contact with the infant, but it does allow the mother to breastfeed (exceptiong is in the cases of Tb mastitis) (4) Certain drugs are secreted in the breast milk and should be avoided (a) Lithium carbonate, tetracycline, bromocriptine, methotrexate, and any radioactive substance iii) Physiology (1) After birth there is a drop in hormones, especially estrogen, that leads to a release of lactation feedback inhibition of prolactin action (2) Oxytocin -> milk let down and is released by stimulation of the nipple ObGyn Beckman 37

(3) Initial secretion is colostrum with IgA which is replaced by day 5 with milk iv) Ongoing production requires adequate insulin, cortisol, and thyroid hormone v) Minimal maternal caloric intake is 1800 kcals/day vi) Nipple care (1) Exposed to air 15-20 minutes postfeeding (2) Water-based cream if nipples are tender 3) Anxiety, Depression, and Postpartum Period a) Postpartum blues: i) Feeling of sadness, anxious, or angry ii) May last 1-2 weeks iii) Tx: support and reassurance b) Postpartum depression i) More severe and longer in duration than the blues ii) Feelings interfere with ADL iii) Younger women are more likely to experience depression than older iv) Increase risk if history of depression during pregnancy c) Postpartum psychosis: i) Women have pre-existing mental disorders ii) Medical emergency 4) Postpartum visit a) Status of breast feeding, return of menses, coital activity, contraception, interaction with newborn, and resumption of physical activities b) Pap smear i) May show some atypia as the cervix is inflamed and begins to heal ii) Unless there is a Hx of atypical pap smears follow up in 3 months ObGyn Chapter 12: Postpartum Hemorrhage 1) Introduction a) Accounts for more than half of maternal deaths within 24 hours b) Sequelae: adult RDS, coagulopathy, shock, and Sheehan syndrome c) PPH delivery associated blood loss i) Vaginal > 500 mL ii) CS >1000 mL iii) 10% drop in hct 2) Recognition and Early Detection a) PPH is not a diagnosis, but an important sign that often occurs without warning and in the absence of risk factors b) Blood loss approaching 20% symptoms i) Tachycardia, tachypnea, delayed capillary refill, orthostatic changes, and narrowed pulse pressure c) Blood loss 40-50% i) Oliguria, shock, coma d) PPH etiology i) Uterine atony (most common), retained placenta, genital tract trauma, ObGyn Beckman 38

coagulation disorders 3) General Management with Postpartum Hemorrhage a) Uterine atony i) Assessed by bogginess of the uterus ii) Tx: oxytocin, methylergivine (IM, because of its potency ->HTN), prostaglandins (hemabate: carboprost and dinoprostone) b) Fluid replacement: large bore IV, crystalloid, blood transfusion, and evaluation for FFP transfusion 4) Major Causes of PPH and their Management a) Uterine Atony: failure of the uterus to contract postpartum to prevent blood loss i) Caused by overextension of the uterus and conditions that interfere with contraction ii) Management: stage 3 labor -> uterine massage, oxytocin, traction on the placental cord, and immediate breastfeeding (endogenous release of oxytocin) (1) Second line intrauterine compression with a balloon (2) Surgical: uterine compression sutures/sequential arterial ligation (3) Last ditch: hysterectomy/iliac artery ligation b) Lacerations of the lower uterine tract i) Risk factors: instrumental deliver, breech extraction, precipitous delivery, non LOA, marcosomia ii) These lacerations do not result in immediate PPH, but can cause PPH if left untreated c) Retained Placenta i) Cleavage occurs between the zone basalis and the zona spongiosa facilitated by uterin contraction ii) Risk factors: CS, uterine leiomyomata, prior uterine curretage, and partial uterine succenturiate iii) Placenta is missing placental cotyledons -> retained in uterus iv) Placenta acreta, increta, and percreta are usually sporadic along the placenta and it will separate in shreds v) Management: (1) Sweeping the uterus for the placenta, curretage, last ditch -> hysterectomy d) Other causes of PPH i) Hematoma: occur along the vuvlva to the upper vagina and are due to birth trauma (1) 5 cm can be monitored and managed with ice packs (2) large and expanding hematomas whether along the site of the episiotomy need to be open, drained, and sutured drains or vaginal packs may be helpful ii) Coagulation Defects: congenital or acquired (DIC) -> correct the deficiency with replacement factors iii) Amniotic Fluid Embolism: five findings in the following order: respiratory distress, cyanosis, cardiovascular collapse, hemorrhage, coma ObGyn Beckman 39

(1) Often results in severe coagulapathy (2) Tx: life support iv) Uterine Inversion (1) Management: uterine replacement (requires tocolytic: terbutaline, halogenated general anesthetics, MgSO4, and nitroglycerin v) Uterine Rupture (1) Risk factors: previous CS/congenital malformation 5) Prevention a) Active management of the third stage of labor: immediate removal of the placenta, and administration of uterotonic agent ObGyn Chapter 13: Ectopic Pregnancy 1) Ectopic pregnancy a) Extrauterine pregnancy -> most common location is the ampulla of the fallopian tube b) Diagnosed by hCG levels and transvaginal US c) Pathophysiology and Risk Factors i) Risk factors: (1) salpingitis and chlamydial infection -> tubal infection (2) Sterilization (3) Contraceptives decrease the likelihood of intrauterine pregnancy thus increasing the relative incidence of ectopic pregnancy d) Symptoms i) Amenorrha followed by vaginal bleeding and abdominal pain ii) Reference pain to the shoulder from diaphragm irritation due to subdiaphragmatic blood iii) Vertigo and syncope -> hypovolemia iv) Abortion bleeding/D and C does not demonstrate chorionic villi then an ectopic implantation should be assumed e) Clinical findings i) Before rupture diagnosis only made by hCG and US ii) After rupture (1) Pelvic tenderness (2) Cervical manipulation tenderness f) Differential diagnosis i) Early pregnancy complications (abortion) ii) Hemorrhagic corpus luteal cyst iii) Placental polyp iv) Normal pregnancy v) Appendicitis vi) Renal caliculi g) Diagnostic procedures i) -hCG (1) Negative urine -hCG excludes ectopic pregnancy (2) Normal -hCG increase rate (a) Log fashion days 60-80 ObGyn Beckman 40

(b) 66% increase observed every 48 hours (c) NOTE; deviation from this rate may indicate an abnormal pregnancy ii) Transvaginal US (1) 5 -6 weeks: cardiac activity (2) Discriminatory value -hCG (a) 1000-2000: Level at which a pregnancy can by seen on TVUS (b) 5000-6000: TAUS (3) Absence of intrauterine pregnancy signifies ectopic pregnancy, incomplete abortion, or complete abortion (4) Pseudogestational sac: intracavitary fluid collection caused by sloughing of the decidua typically situated in midline (a) Normal gestational ac usually sits eccentric iii) Progesterone levels (1) < 5 ng/mL identifies a nonviable pregnancy (2) >20 ng/mL healthy pregnancy iv) Curretage (1) + Chorionic villi -> intrauterine pregnancy (2) Chorionic villi -> extrauterine pregnancy v) Arias-Stella reaction: hypersecretion of the endometrium occurs in both ectopic and intrauterine pregnancy vi) Culdocentesis (1) Identify hemoperitoneum (non-clotting blood) (a) If positive warrants the need for further evaluation vii) Laproscopy -> most accurate (1) May mistaken a hematosalpinx for an ectopic viii) Management (1) Medical: methotrexate (a) Women have to be in no acute distress (b) Relative contraindications: fetus >3.5 cm and embryonic cardiac motion (c) Works best when -hCG < 5000 (d) Side effects: N/V, diarrhea, gastric distress, dizziness, or stomatitis (i) Abdominal pain that can be controlled with NSAIDS (e) Follow up on day 4 and 7 on -hCG levels (should decrease) (2) Rh negative mothers should receive rhogam 2) Types of Ectopic Pregnancy a) Tubal pregnancy i) Tubal abortion: expulsion of the conceptus into the abdominal cavity which may result in abdominal implantation ii) Tubal rupture: associated with intra-abdominal hemorrhage iii) Medical management: same as any ectopic pregnancy iv) Surgical management (1) Linear salpingostomy -> removal of the pregnancy (2) Segmental resection -> removal of the affected section (3) Salpingectomy -> removal of the entire tube ObGyn Beckman 41

b) Ovarian pregnancy i) Dx: US -> cyst with a wide echogenic outer ring on or within the ovary c) Interstitial pregnancy (corneal/isthmus pregnancy) i) Location where the uterus and tubes meet ii) May make it to week 8-16 iii) Rupture -> massive hemorrhage usually ending in hysterectomy d) Cervical pregnancy i) Implants below the level of the internal os ii) Risk factor: Hx of D and C iii) Two diagnostic criteria (1) Cervical glands opposite the placental attachment (2) The placenta lies below the uterine vessels or the reflection on the A/P surface e) Heterotopic pregnancy i) Coexistence of an ectopic and intrauterine pregnancy ii) Management: surgical/medical (injection of KCl into the pregnancy sac) f) Abdominal Pregnancy i) Tx: surgical removal of the pregnancy or carrying the fetus to viability than operative delivery 3) Spontaneous Abortion a) Abortion: expulsion of the uterus before 20 weeks b) First trimester: chromosome abnormalities c) Second trimester: maternal disease, abnormal placenta, or other anatomic considerations d) Etiology i) Infectious: C. trachomatis, L. monocytogenes, GBS ii) Endocrine: Thyroid antibodies, type I diabetes iii) Environmental: cigarettes, radiation (< 5 rads doesnt increase risk of abortion iv) Immunologic: thrombophilias v) Uterine: leiomyomas (location being a strong determining factor), intrauterine synechiae (history of curretage) 4) Classifications of Spontaneous abortions a) Threatened abortion: normal US with minimal bleeding and withour cervical dilation. Tx: observation b) Inevitable abortion: heavy bleeding, cervical dilation and expulsion of the products of the coneptus i) Incomplete abortion: heavy bleeding, cervical dilation, and expulsion of PART of the products of conceptus ii) Complete abortion: heavy bleeding, cervical dilation, and expulsion of the ENTIRE product of conceptus c) Missed abortion: retention of a failed intrauterine pregnancy without bleeding or cervical dilation d) Septic abortion: Hx of nonsterile abortion and attempted resulting in uterine infection. Tx: hospitalization and treatment with broad spectrum antibiotics e) NOTE: Rh negative moms require rhogam ObGyn Beckman 42

5) Recurrent pregnancy loss a) First trimester: chromosome problems b) Second trimester: i) Maternal anamolies (1) Septate uteris (2) Intrauterine synechiae (3) Asherman syndrome: amenorrhea, irregular bleeding, infertility and recurrent pregnancy loss (a) Associated with intrauterine synechiae -> post D and C (b) Tx: estrogen to regain normal endometrium (4) Antiphospholipid Ab: Tx. Low dose aspirin and infractionated heparin 6) Induced Abortion a) First trimester: D and C (sunction curretage or vacuum aspiration) b) Second trimester: sunction/extraction forceps or prostaglandins c) Outpatient medical abortion i) Pregnancies less than 49 days of gestation ii) Mifepristone: antiprogestin (remove contraction inhibition) iii) Methotrexate: antimetabolite (remove contraction inhibition) iv) Misoprostol: prostaglandin (stimulate myometrium) v) May not always be complete and require D and C d) Surgical e) Complications: uterine perforation, cervical laceration, hemorrhage, incomplete removal of the fetus/placenta, and infection ObGyn Chapter 16: Hypertension in Pregnancy 1) Classifications a) Chronic HTN: begins before 20 weeks gestation or was present before pregnancy i) Mild: Systolic 140-180 or diastolic 90-100 ii) Severe: systolic 180 or diastolic 100 iii) May progress to preeclampia/eclampsia b) Gestational HTN: begins after 20 weeks gestation and returns to normal after delivery of the fetus i) May also have preeclampsia/eclampsia superimposed ii) Because of the severity of preeclampsia need to work up for preeclampsia c) Preeclampsia i) Triad -> HTN (systolic 140; diastolic 90), proteinuria (0.3 grams over 24 hour period, edema (note other symptoms may be presenting but these are the major symptoms) ii) If severe only treatment is delivery of the fetus d) Eclampsia i) HTN, proteinuria, edema, and convulsions (grand mal seizures) e) HELLP syndrome (derivative of preeclampsia) i) Hemolysis (microangiopathic), Elevated Liver enzymes, Low Platelets 2) Pathophysiology of Pregnant HTN ObGyn Beckman 43

a) Etiology of gestation HTN and preeclampsia is maternal vasospasm i) Vascular changes, hemostatic changes, increase in lipid peroxide, free radicals, and antioxidant release: (1) Changes in endothelium dynamics favoring vasospasm ii) Prostaglandins: shift to favoring thrombaxane production -> vasospasm iii) Changes in endothelium derived factors: nitric oxide decreases -> vasospasm b) Pathophysiologic changes i) CV: elevated blood pressure and increase in CO ii) Hematologic: plasma volume contraction -> increase in hematocrit values; DIC -> microangiopathic hemolytic anemia iii) Renal: decrease in GFR -> increase in BUN and Creatine; Proteinuria; atherosclerotic changes in glomerular vessels iv) Neurologic: hyperreflexia, hypersensitivity v) Pulmonary: decrease colloid pressure -> edema vi) Fetal: intrauterine growth retardation and increase risk of placental abruption 3) Evaluation a) H and P i) Visual changes -> scotoma (vasoconstriction of retinal blood vessels) ii) Persistent headache b) BP standing > sitting > lying in the lateral position c) BP normal trend: decrease in the second trimester and then rise back in the third trimester d) Rapid weight gain -> edema 4) Management a) Chronic HTN i) Treatment is only given in cases for severe HTN ii) Methyldopa, alpa/beta blocker, calcium channel blockers, diuretics b) Preeclampsia i) Mild: bed rest and close monitoring (fetal growth restriction an doligohydroamnios) ii) Severe/worsening: hospitalization, daily monitoring, magnesium sulfate and antihypertensive medications as needed iii) Magnesium sulfate (1) To prevent eclamptic seizures (2) Therapeutic leveles 4-6 mg/dL (greater than equals toxic complications) (3) Monitor patellar reflex and respirations (4) Reversal of toxic levels -> calcium gluconate iv) Antihypertensives (1) First use hydrazaline (goal to decrease diastolic pressure to 90-100) (2) Labetalol v) After seizures and HTN are under control thought towards induction of labor is begun c) Eclampsia ObGyn Beckman 44

i) Risk for biting of the tongue, hypoxia, and aspiration ii) Seizures are usually limited and magnesium sulfate should be started (1) Other anticonvulsants are not warranted iii) Transient uterine hyperactivity iv) Mom is too unstable to deliver at this point d) HELLP Syndrome i) Monitoring and platelet transfusion ObGyn Chapter 17: Multifetal Gestations 1) Natural History of monozygotic twinning a) Diamnionic/dichorionic i) Division of the conceptus within three days b) Diamnonic/monochorionic i) Division between days 4 and 8 c) Monoamnionic/monochrionic i) Division occurs between days 9 and 12 ii) Division after 12 days may lead to conjoined twins (1) Most common site of fusion is the chest/abdomen 2) Risks of multifetal gestation a) Increase in prenatal morbidity (3-4x) -> preterm labor and delivery b) For each extra fetus in the length of gestation is decreased by 4 weeks i) Twins 37 wks, triplets 33 wks, quadruplets 29 wks c) Increase risk of preeclampsia, placental abruption, and umbilical cord accidents d) Twin-twin transfusion i) Monochorionic development of vascular anastamoses ii) Donor twin: impaired growth, hypovolemia (1) Hypovolemia -> oligohydroamnios iii) Recipient twin: HTN, polycythemia, CHF (1) Hypervolemia -> increase urine output -> preterm labor iv) Tx: removal of amniotic fluid/laser ablation of anastamoses v) May have an absent of one umbilical artery which is indicative for renal agenesis e) Death of one fetus i) Maternal cause: delivery of the other fetus is warranted ii) Fetal cause: continue to carry the other fetus to full term with carefule monitoring iii) Complication with monochorionic twins: share a placenta so the other twin will experience placental hypotension -> complications and death 3) Diagnosis and Antenatal Management a) Diagnosed with US b) Suspected with uterus size is greater than estimated gestation age c) First trimester i) 50% make it to delivery ii) 50% deliver a singleton pregnancy because of fetal demise and ObGyn Beckman 45

reabsoprtion (vanishing twin) iii) Monitor these patients more closely d) US every 4 weeks beginning at week 16-18 4) Intrapatum management a) Presenting twin in cephalic vertex position may vaginal deliver b) Presenting twin in breech position requires CS c) Second twin in cepahilc vertex -> vaginal deliver d) Second twin in breech position -> external cephalic version, deliver via breech, or CS e) Increase risk of uterine atony and hemorrhage ObGyn Chapter 19: Isoimmunization 1) Issoimunization: development of maternal antibodies to blood products that can lead to transplacental passage of these antibodies and destroy fetal red blood cells a) Hemolytic disease of the newborn: hemolysis, bilirubin release, and anemia 2) Natural History a) Most common antigen involved part of the Rh system specifically the D antigen b) More common in caucasions to be Rh negative c) Variant of Rh negative is weak D antigen diagnosed incorrectly as Rh negative d) Minimal amount of blood required to cause issoimmunization is 0.1mL 3) Effects of Ab Development of the Fetus a) First effected pregnancy can suffer from mild anemia and elevated bilirubin at birth. If severe enough can cause kernicterus b) Tx: UV light and exchange transfusion c) Fetal anemia increases with subsequent pregnancies due to a anamnestic response d) Severe anemia can lead to hydrops fetalis -> third spaceing and high-output cardiac failure 4) Zones of fetal anemia a) Zone 1: mildly affected follow amnio q2-3 weeks b) Zone 2: moderately affected follow amnio q1-2 weeks c) Zone 3: severe anemia PUBS 5) Treatment a) First pregnancy -> rhogam postpartum within 72 hours b) Second pregnancy -> rhogam at 28 weeks and at the time of pregnancy (if more than 12 weeks has passed from the last dose) 6) Assessment a) Critical titer at 1:8 and 1:32 -> significant risk for fetal hemolytic disease b) Titers at 1:8 may be monitored every four weeks c) Fetus Monitoring i) Serial bilirubin levels of the amniotic fluid -> elevation in bilirubin is indicative of progressive disease ObGyn Beckman 46

ii) Measurement of the peak velocity MCA flowing using Doppler ultrasound (1) Anemia -> decrease viscosity -> decrease velocity (2) US: hydropic changes -> third spacing (3) PUBS: if severe anemia is determined to determine fetal hct (average is 36-44% d) Tx: transfusion through the umbilical vein of Rh negative cells, after 2-3 units the fetal blood is completely from the transfusion 7) Rhogam a) 300 micrograms of rhogam neutralizes 30 mL of fetal blood and 15 mL of RBC b) Cases where more than 30 mL of fetal blood has crossed usage of the Kleihaur-Best test can be used to determine the amount of fetal blood that was crossed and rhogam dosing adjusted accordingly 8) Kell antigen a) Another antigen of isoimmunization that can lead to hemolytic disease of the newborn 9) ABO hemolytic disease a) Less common because of fewer A and B antigens on fetal RBC and the major isoform is IgM ObGyn Chapter 20: Preterm Labor 1) Introduction a) Preterm labor (uterine contractions with cervical change): delivery before 37 weeks gestation b) Preterm common complications: i) RDS, intraventricular hemorrhage, necrotizing entercolitis, sepsis, neurologic impairment, and seizures c) Preterm births are either spontaneous/indicated and may result from preterm labor, preterm PROM, and deliberate intervention 2) Cause of Preterm Labor a) Activation of the maternal/fetal hypothalamic-pituitary-adrenal axis due to maternal/fetal stress b) Decidua/chorioamniotic inflammation (i.e. infection) c) Pathologic uterine distension d) Decidual hemorrhage e) Risk factors: multigestation (strongest risk factor), prior preterm birth, preterm PROM f) Decrease in mortality of preterm birth is due to advances in NICU, administration of steroids for RDS and intraventricular hemorrhage, and tocolytics that delay labor 48 hours to allow the steroids to take the full effect 3) Prediction of Preterm Labor a) Fetal fibronectin levels (fFN) i) Rises as pregnancy approaches term, and can predict labor within 7-14 days ii) It has a low positive predictive value and a high negative predictive value ObGyn Beckman 47

-> indicating it is a good rule out preterm labor not rule in b) Cervical length (TVUS) i) Decrease in midpregnancy has been shown to have an increase risk for preterm birth c) Cervical insufficiency d) Bacterial Vaginosis i) Associated with preterm birth and preterm PROM 4) Prevention of Preterm Labor a) Injections of progesterone starting at 16-20 weeks of gestation and continuing until 36 weeks appears to reduce spontaneous preterm labor 5) Evaluation of a Patient in Suspected Preterm Labor a) Monitoring of contractions and sterile speculum exam for cervical change b) Labs: Urine culture & UA (UTI may induce uterine contraction), vaginal/rectal GBS culture (prophylaxis), Chlamydia and Niesseria cultures, amniocentesis culture (infection) 6) Management of Preterm Labor a) MgSO4, indomethacin, calcium channel blocker (procradia/nefidipine), agonist (ritodrine, terbutaline) ObGyn Chapter 21: Third-Trimester Bleeding 1) Introduction a) Differential: placenta previa, placental abruption, vasa previa, uterine rupture, and preterm labor b) 20% of maternal blood is shunted to the uterus and hemorrhage is the leading cause of fetal morbidity and mortality c) Post-coital bleeding is not uncommon because of increase vascularity of the cervix d) Management: IVF, crystalloid fluid, CBC, coagulation profile, type and cros four units, and Kleihauer-Betke test, and prepare for CS 2) Placental Previa a) Placenta location close to the cervical internal os b) Four types i) Complete: covers the entire internal os ii) Partial: covers partial of the internal os iii) Marginal: placenta is on the edge of the internal os iv) Low-lying: near the internal os (1) NOTE: second trimester marginal/low-lying placenta may be reevaluated at 32-35 weeks for transmigration c) CP: painless vaginal bleeding that ceases within 1-2 hours d) Management: US FIRST, speculum examination, bimanual examination i) If stable outpatient management until 37/38 weeks and then CS delivery ii) Unstable CS e) Complications: increase risk for placenta acreta, increta, and percreta 3) Placental Abruption ObGyn Beckman 48

a) Premature separation of the placenta from the uterus b) Three types i) Complete, partial, or marginal (around the edges) c) Concealed hemorrhage: the placenta is ruptured, but the bleeding is in between the placenta and the uterus -> no noticeable hemorrhage d) CP: vaginal bleeding with abdominal pain e) Risk Factors i) Chronic HTN, preecalampsia, multiple gestation, maternal age, multipartiy, smoking, cocaine, chorioamnionitis, and trauma f) Second trimester elevation of AFP 10x increase in placental abruption g) Cauvelaire uterus: blood penetrates the uterus to the extent that the serosa turns blue h) Complications: coagulopathy (hypofibrinogen), hemorrhage, DIC i) Management: i) Maternal ABC ii) Rhogam for Rh negative Mom iii) CS 4) Vasa Previa a) Passage of fetal blood vessels over the internal os below the presenting part of the fetus i) May occur with velamentous insertion in which the fetal blood vessels insert btw. the amnion and chorion b) Rupture of the vessels can quickly lead to fetal exsanguination c) Cutting the umbilical artery usually occurs with artificial ROM with an unengaged fetal part i) CP: strong flow of blood with an immediate drop in FHR d) May use Apt test to distinguish between maternal and fetal blood e) Management: emergency CS 5) Uterine Rupture a) Most commonly associated with prior CS b) Parital rupture (uterine dehiscence): peritoneum remains intact c) Management: CS ObGyn Chapter 22: Premature Rupture of Membranes (PROM) 1) Introduction a) Amniotic fluid role protect against infection, trauma, umbilical cord compression, incomplete alveolar development b) PROM: rupture of the membranes before onset of labor c) Preterm PROM: rupture of membranes before the onset of labor and 37 weeks -> leading cause of neonatal mortality d) Complications: infection, umbilical cord prolapse, and placental abruption 2) Etiology a) Lower gentical tract infection -> bacterial products and prostaglandin synthesis weaken fetal membranes and stimulate uterine contraction b) Risk Factors: smoking, prior PROM, short cervical length, prior preterm ObGyn Beckman 49

labor, hydroamnios, and multiple gestations c) Chorioamnionitis: inflammation of the membranes 3) Diagnosis a) Fluid passing through the vagina must by presumed to be amniotic fluid until proven otherwise b) Nitrazine test: increase in vaginal pH c) Fern test: amniotic fluid upon drying will demonstrate a fern pattern d) US: decrease in the amount of fluid on US, or transabdominal istillation of indigo carnine dye and observation of the dye in the vagina 4) Evaluation and Management a) Sterile speculum examination, cultures, , observation of the pooling of fluid, and examination for amniotic fluid b) NOTE: digital examination should be kept to a minimum to maintain sterility c) Page 216 Table 22.2 ObGyn Chapter 24: Contraception 1) Hormonal Contraceptives a) Oral i) Benefits: (1) Decrease risk of ovarian and uterine cancer (2) Shorter, more predictable, less painful periods ii) Mechanism of Action (1) Progesterone: (a) Suppressing the secretion of LH and ovulation (b) Thickening cervical mucous (c) Altering fallopian tube persitalsis (2) Estrogen (a) Suppresses FSH secretion and the maturation of the follicle iii) Progestin only pills (1) MOA: thicken cervical mucus and make it relatively impermeable (2) 40% still ovulate (3) Effective for women who are breastfeeding, over the age of 40, or where estrogen containing pills are contraindicated (increase risk for thrombosis) (4) > 3 hours late in taking a pill backup contraception should be used for 48 hours iv) Complications: (1) Break through bleeding within the first few months ->normal (most common reason for discontinuation) (2) Break through bleeding > 3 months indicates decidua growth and break down and can be treated with estrogen (3) Amenorrhea -> normal develops after one year, but may need to add exogenous estrogen so the women cycles and is more reassured. Need to have pregnancy test beforehand (4) Post-pill amenhorrhea ObGyn Beckman 50

(5) Serious (a) DVT, cholestasis, stroke, MI, hepatic adenoma with high dose formulations v) Contraindicated (1) Women who are 35 or older and smoke (2) Women who have had a thromboembolism (3) Women with a history of CVD b) Transdermal contraceptive patch i) Women greater than 198 lbs (90 kg) has decrease efficacy ii) Complaints: skin irritation and adhesive residue c) Contraceptive vaginal ring i) Decrease incidence of breakthrough bleeding d) Depo medroxyprogesterone acetate i) Injections every three months ii) Given within the first five days of menstruation iii) Lock of estrogen iv) FSH suppression does not occur v) Alteration of bone metabolism -> decreasing bone mineral density vi) Efficacy is equivalent to sterilization vii) Lack of a period leads some women to discontinue use -> may take 6 months to one year to regain menses (>1 year should be evaluated further) e) Implant contraceptive i) Has both estrogen and progestin ii) Problems: irregular bleeding 2) Barrier Complications a) Condoms, diaphragm, and cervical cap b) Oil based lubricants are contraindicated due to degradation of the latex c) Only latex condoms protect against HIV d) Diaphragm i) Insert 6-8 hours before intercourse, left in place 6-8 hours after intercourse, and not left in more than 24 hours ii) If intercourse is desired during the 6-8 hours post coital more spermicide must be applied and the waiting period restarted iii) Twice as likely to develop a UTI incomparison to those on hormonal contraceptives e) Cervical cap i) Similar to the diaphragm ii) Associated with a high degree of displacement, cervicitis, and TSS f) Sponge i) Has spermicide, inserted prior to intercourse, associated with TSS 3) Spermicides a) Nonoxynol-9 b) With condoms has a failure rate the approached oral contraceptives c) Applied before intercourse and left in for 8 hours post intercourse 4) Intrauterine Contraceptives ObGyn Beckman 51

a) Levonorgestrel i) Better effectiveness than the copper ii) Has the benefits of the hormone contraceptive b) Copper i) Can also be used as an emergency contraception c) Infection i) May occur due to introduction from the procedure or STD ii) If one does occur treat with antibiotics and the device does not have to be removed iii) Increase in the relative risk of an extra-uterine preganancy iv) Pregnancy does occur it will spontaneously abort, or begin to mature (1) Intrauterine pregnancy doe occur with expulsion remove the IUD if not leave it in (2) Increase risk for preterm labor d) Best time to place it is during menstruation 5) Natural Family Planning a) Knowing the time of ovulation and either obstaining or using barrier contraceptives during this time b) Requires a female with a stable cycle c) May use the following methods i) Calendar (fertile cycle day 10-17), basal body temp. (increase in basal body temperature 0.5-1 degree Celsius), cervical mucus (thinning), symptomthermal (combome bof BBT and cervical mucus) d) Most complications in reading cycle comes postpartum because women begin ovulating before they resume menstruation 6) Post-coital emergency contraception a) Plan B i) Taking two tablets (progestin only -> levonorgestrel) twice over a 24 hour period ii) Prevents ovulation and fertilization and will not terminate an already existing pregnancy b) Copper IUD (lesser failure rate than Plan B) this requires a previous pregnancy test prior to prevent the removal of an already implanted pregnancy ObGyn Chapter 25 Sterilization 1) Sterilization of Men a) Vasectomy: excision and ligation, electrocautery, and mechanical and chemical occlusion of the vas deferens i) Safer, less evasive, and more easily reversed ii) Is not an immediate sterilization iii) 50% at 8 weeks and 100% at 10 weeks 2) Sterilization of Women a) Surgical sterilization; can occur after D and C, CS, or vaginal delivery b) Failure rates are about equal to that of an IUD c) Pregnancy needs to be ruled out before sterilization ObGyn Beckman 52

d) Laparoscopy i) Electrocautery (unipolar/bipolar) (1) Inadvertent electrical damage, poorer reversibility, and greater incidence of ectopics (2) Bipolar is safer than unipolar and (3) Unipolar has a lower failure rate ii) Flishie clip (plastic/spring clip) (1) Similar to the Falope ring iii) Hulka clip (1) Readily reversible, but has the greatest risk of failure iv) Silastic Band (Yoon/Falope ring) (1) Intermediate for reversibility and failure rate (2) Increase incidence of post-operative pain v) Aiming for the isthmus of the fallopian tube e) Minilaparotomy i) Most common form of tubal ligation ii) Occlusion using methods similar to laparoscopy, removal of all or part of the fallopian tube (Pomery tubal ligation -> make a loop, cut it out, seal the ends (1) After removal of the tube it should be sent for histology to confirm that it is not the round ligament f) Transvaginal g) Hysteroscopy i) Transcervical approach ii) Placement of titanium-Dacron spring device directly into the tubal ostia bilaterally -> tubal reaction that leads to occlusion iii) Pretreat with DMPA or Combined pills to thin mucus iv) Need hysteroscopy to confirm occlusion h) Side effects i) Infection, bleeding, injury to the surrounding structures ii) Post-sterilization pregnancies will be ectopic (1) Most common in cautery based sterilization because of the formation of fistulas i) Decrease lifetime risk of ovarian cancer and it may offer some protection from PID 3) Reversal of Tubal ligation a) Suggest IVF instead of reversal ObGyn Chapter 25: Vulvovaginitis 1) Introduction a) Vulvovaginitis: spectrum of vaginal and vulvar symptoms such as itching, buring, irritation, and abnormal discharge b) Etiology i) Bacterial vaginosis > vulvovaginal candidiasis > trichomoniasis c) Focused history ObGyn Beckman 53

2)

3)

4)

5)

i) Discharge, vaginal malodor, itching, irritation, burning, swelling, dyspareunia, and dysuria, relation to mestrual cycle, and response to prier treatment d) Test i) Vaginal pH, amine (whiff) test,wet mount, 10% KOH Normal vulvovaginal ecosystem a) Puberty: vagina enriches with glycogen and favoring the growth of lactobacilli i) Bacteria change the glycogen to lactic acid lowering the pH of the vagina b) Vaginal discharge i) Majority normally mucus from the cervix, skene and bartholin gland secretions, exfoliated squamos cells, secretions from the vagina (off white color) -> have not odor Bacterial Vaginosis a) Polymicrobial infection -> caused by a decrease in lactobacilli and an overgrowth of anaerobic bacteria (Gardenalla vaginalis most common etiology -> clue cells) i) CP: (1) Fishy-musty odor discharge (2) Discharge is grey to yellow (3) Increase in vaginal pH > 4.5 ii) Diagnost criteria (1) Gray discharge (2) pH > 4.5 (3) Positive wiff test (4) Clue cells iii) Tx: oral metronidazole or topical clindamycin Vulvovaginal Candidiasis a) Etiology: C. albicans b) More likely in immunosuppressed, diabetic, obese, on OCP, broad spectrum antibiotics c) CP: i) Odorless cottage cheese discharge d) Tx: OTC treatments i) Those on OTC treatments need to stop 3 days before office visit ii) Topical treatment with and azole iii) Oral therapy low dose fluconazole (note pregnant women get the topical azole b/c fluconazole is associated with birth defects) e) Recurrent infection may be treated with low does oral fluconazole for 6 months to prevent recurrences f) Dx: visualization of the spores/ pseudohyphae on a wet mount or KOH prep Trichomonas Vulvovaginitis a) T. vaginalis: Flagellate protozoa b) Transmitted through sexual contact or fomites (swimming pools) c) Complications: PID, endometritis, ectopic pregnancy, etc. d) Facilitates HIV infection ObGyn Beckman 54

e) CP i) Copious rancid discharge; FROTHY discharge; pH > 4.5 ii) Dysuria, dyspareunia iii) Strawberrycervix f) Dx: wet mount visualization of the protozoa g) Tx: metronidazole/tinidazole 6) Atrophic Vaginitis a) Atrophy of the vagina due to a decrease in estrogen (prepubertal/postmenopausal) b) Decrease in estrogen -> decrease in glycogen -> decrease in lactic acid c) Vagina is thin, pH >4.7 d) CP: dryness, itching, burning e) Tx: topical or oral estrogen 7) Desquamative Inflammatory Vaginitis a) Perimenopausal women b) Exfoliation of the epithelium, vulvovaginal burning, erythema, decrease in lactobacilli and overgrowth of G+ cocci c) pH > 4.5 d) Tx: clindamycin cream for 14 days ObGyn Chapter 27: Sexual Transmitted Diseases 1) Screening: testing positive for one STD indicates screening for all STD 2) Expedited partner therapy: a patients sexual partner receives drug therapy for an STD without undergoing physical examination or testing. 3) Summary of Infections Table 27.1 Page 249 4) Chlamydia trochomatis a) Gram negative intracellular obligate bacterium that lacks the metabolic ability to produce ATP b) 40% of untreated cases will develop PID c) Disease: nongonococcal urethritis/inclusion conjunctivitis d) All cases under the age of 25 should be screened annually e) Symptoms i) Mucopurulent cervicitis that may ascend into a salpingitis f) Diagnosis i) Culture, PCR, NAAT g) Treatment i) Azythromycin (one dose), doxycycline (7 days) ii) Non-compliant/re-infected patients require a test of cure iii) All women should be retested 3 months after treatment 5) Niesseria gonorrhea a) Gram negative intracellular diplococcus b) Highest rates of infection are seen in adolescents and young adults c) Infection may facilitate transmission of HIV d) Symptoms i) Urethritis (men); cervicitis (women) ObGyn Beckman 55

ii) Infection of the Bartholin glands is common e) Diagnosis i) Culture, PCR, or NAAT ii) Culture is the preferred method of diagnosis for the rectum/pharynx f) Treatment i) Ceftriaxone, cefixime, ciprofloxacin ii) Note: high quinolone resistance 6) Pelvic Inflammatory Disease a) Infection of the upper genital tract and spread along mucosal surfaces b) Most common bugs C. trachomatis, N. gonorrhea c) Endocervical mucous resist movement of the ascending bacteria i) Mucous is most thickened during the progesterone stage of the cycle ii) OCP also increase mucous and decrease likelihood of PID d) Risk Factor i) Prior PID, untreated chlamydia and gonorrhea e) Diagnosis i) Differential (1) Ectopic pregnancy, septic incomplete abortion, acute appendicitis ii) Clinical Diagnosis (1) Discharge, pelvic tenderness, and cervical motion tenderness, adnexal tenderness iii) Complications (1) Fits Hugh Curtis syndrome - perihepatitis (2) Tuboovarian abscess (acutely ill) f) Treatment i) Oral/IV antibiotics ii) TOA: surgical drainage may be even hysterectomy 7) Genital Herpes a) HSV (DNA virus) b) Oral Herpes HSV-1; Genital Herpes HSV-2 c) Symptoms i) First episode is accompanied by a flu-like symptoms ii) Vesicular lesions -> lyse and progress to shallow ulcers (1) Are extremely tender iii) May progress to asceptic meningitis d) Diagnosis i) Viral culture, PCR (more sensitive) e) Treatment i) Antivirals (acyclovir), analgesics, stiz baths ii) Episodic therapy: anti-virals decrease the duration of the episode iii) Suppresive therapy: (works in 80% of cases) iv) CS for pregnant women in times of prodrome/outbreak 8) HPV a) Occurring in up to 80% of sexually active women b) Spread by skin to skin contact c) HPV 6 and 11 are associated with condyloma acuminata (low risk) ObGyn Beckman 56

d) HPYV 16, 18, 31, 33, and 45 are high risk e) Condyloma acuminata i) Diagnosis (1) CP and biopsy of warts ii) Treatment (1) Patient applied: podofilox, imiquimod (2) Healthcare provider: trichloroacetic acid, podophyllin resin, laser, surgical removal (3) Lesions > 2 cm respond best to cryotherapy, cautery, or laser treatment iii) Pregnant women: CS to avoid fetal transmission of laryngeal papilloma f) Cervical Dysplasia i) Associated with high risk HPV 16 and 18 ii) HPV vaccine is recommended for all women ages 9 to 26 to be immunized 9) Syphillis a) Treponema pallidum: anaerobic spirochete b) Symptoms i) Primary: painless chancre (serologic testing at this time is negative) ii) Secondary: rough red/brown lesions on the hands and feet and condyloma lata (flat top papules which coalesce) iii) Latent phase iv) Tertieary: sexual transmission unlikely, but may have transmission via blood or placenta (1) Gummas of the CNS and cardiovascular system c) Diagnosis i) Dark field microscopy and direct fluorescent antibody ii) VDRL/RPR d) Treatment i) Benzathine penicillin G ii) VDRL titers and follow up 10)HIV (AIDS) a) RNA retrovirus b) Depletes CD4 T cells c) Black women 24-44 3rd leading COD d) Screening/Diagnosis i) ELSIA confirmed by western blot e) Prevention i) Condoms and safe sex practices f) Treatment i) HAART therapy: NRTI, NNRTI, protease inhibitors 11)Other STDs a) Granuloma inguinale i) Klebsiella granulomatis ii) Lesions are vascular and bleed on contact iii) Clinically diagnosed and confirmed by special stains b) Lymphogranuloma venerum ObGyn Beckman 57

i) C. trachomatis (L1-L3) ii) CP: inguinal or femoral lymphadenopathy +/- genital/anal ulcer iii) Systemic infection if left untreated may cause a secondary infection of rectal/anal lesions which bay lead to abscess or fistulas c) Chancroid i) Haemophilus ducreyi ii) Genital ulcers in distinct outbreaks iii) Diagnosis: PCR d) Molluscum contagiosum i) Contagious viral skin infection ii) CP: small painless papules iii) Tx: antivirals and topical preparations e) Parasitic infections i) Pediculosis pubis (pubic lice) and Scabies ii) Itching of the pubic area ObGyn Chapter 29: Endometriosis 1) Endometriosis: is the presence of endometrial glands and stroma in extrauterine sites a) Occurs more often in women who have never had children 2) Pathogenesis (three theories) a) Retrograde menstruation b) Vascular and lymphatic dissemination c) Coelomic metaplasia 3) Pathology a) Typically found on the ovaries in most patients i) Other common areas: pouch of Douglas, round ligament, fallopian tubes, and the sigmoid colon b) Gross appearance i) Mulberry brown ii) Chocolate cyst (ovary) iii) Dark-red or blue domes 4) Signs and Symptoms a) Classic symptoms are dysmenorrhea and deep dyspareunia; depth of invasion is more determinant of severity of disease b) Dysmenorrheal is unrelenting to OCP and NSAIDs, dyspareunia is associated with disease of pouch of Douglas, and uterosacral ligaments c) Infertility is more frequent in women with endometriosis (some asymptomatic women with infertility are later found to have endometriosis) d) Less common: rectal bleeding, dyschezia (painful BM), and hematuria (associated with invasion into these anatomical structures e) PE: classic sign is uterosacral nodularity 5) Diagnosis a) Direct visualization on laproscopy confirmed by histology b) Histological criteria ObGyn Beckman 58

i) Endometrial epithelium, glands, and strome ii) Hemosiderin macrophages c) +/- moderate increase in CA 125, but is not diagnostic d) Imaging: US or MRI 6) Treatment a) Medical: i) OCP (no withdraw pills work best) and NSAIDs ii) DMPA: progesterone only decreasing GnRH release and cycling (1) Side effects: bone mineral loss -> need to consider patients risk for osteoporosis iii) Danazol: suppressing FSH and LH release (1) Side effects: hypoestrogen and androgenic properties (may not resolve with discontinuation of the drug) iv) GnRH agonist: suppression of FSH and LH (1) Side effects: are fewer than danazol (i.e. androgenic effects are eliminated) v) Add-back therapy (1) Addition of OCP or medroxyprogesterone for GnRH agonist therapy, therapy last longer than 6 months, or if repeated treatments are required vi) Doesnt affect adhesions and fibrosis b) Surgical: i) Conservative (1) Excision, cauterization, or ablation -> allows for future pregnancy (2) Preserve fertility (3) May choose to add medical therapy ii) Extirpative (1) TAHBSO (2) Reserved for severe disease, or when the female no longer desires children (3) Leaving the ovaries has an increase risk of recurrent endometriosis c) No treatment is a cure d) Goal of treatment: decrease pelvic pain, minimize surgical intervention, preserving fertility ObGyn 30: Dysmenorrhea and Chronic Pelvic Pain 1) Introduction a) Dysmenorrhea: painful mestruation preventing a woman from normal daily activities i) Secondary: due to a clinically acceptable cause ii) Primary: excess prostaglanding release b) Chronic Pelvic Pain: non-cyclic pelvic pain that lasts for 6 months or more 2) Dysmenorrhea a) Primary dysmenorrhea i) Does not occur until ovulation begins ObGyn Beckman 59

ii) Greatest incidence in women in their late teens to early 20s iii) Excess PGF2 produced in the endometrium (1) Potent inducer of smooth muscle contraction not only of the uterus, but also smooth muscle elsewhere (GI) iv) NOTE: PGE2 is a vasodilator and inhibits platelet aggregation -> implicated in menorrhagia v) Symptoms (1) Lower abdominal pain that comes and goes related to N/V and diarrhea vi) Treatment: (1) NSAIDs (ibuprofen, naproxen, mefenamic acid (2) Topical heat therapy (3) Intractable primary dysmenorrhea: presacral neurectomy (a) Removal of the superior hypogastric plexus b) Secondary dysmenorrhea i) More common as women age ii) Etiology (1) Endometriosis, adenomysosis, PID, leiomyomata iii) Symptoms (1) Pain may come before and last longer than the menstrual cycle c) Differentiate between the two by the H and P i) Secondary dysmenorrhea (1) Uterine leiomyomata: bimanual exam smooth contour and rubbery consistency (2) Adenomyosis: boggy uterus (3) Endometriosis: painful nodules in the posterior cul-de-sac (4) Confirm by histology ii) Primary dysmenorrheal: normal PE 3) Chronic Pelvic Pain a) When evaluating requires a strong H and P b) Diagnosis of the etiology is hard because it covers a wide range of medical fields c) Pelvic inflammatory disease i) 18-35% of cases will develop chronic pelvic pain d) Irritable Bowel Syndrome i) 50-80% with chronic pelvic pain ii) Diagnosis -> Rome II criteria (1) Abdominopelvic pain for 12 weeks in the preceding 12 months (2) Relieved with defecation (3) Onset associated with change in BM (diarrhea/constipation) (4) Onset associated with change in the type of stool e) Interstitial cystitis i) Chronic inflammatory condition of the bladder ii) Etiology: disruption of glycosaminoglycans layer that coats the mucosa of the bladder f) Therapy ObGyn Beckman 60

i) NSAIDs on a fixed time schedule ii) GnRH agonist offers a therpeuatic modality or diagnostic tool iii) GI workup (IBS, celiac, food allergy) iv) Interstitial cystitis (1) DMSO, pentosan polysulfate (GAG analogue to reestablish the mucosa) v) Hysterectomy -> after all other etiologies have been ruled out leaving only gyn etiologies left. 1) Anatomy a) Young age the breast is glandular, but as one ages the glands are replaced by fat b) Cancer begins in the terminal ducts and then followa the path of the ducts c) Extra breast tissue (polymastia)/ extra nipples (polythelia) may occur anywhere along the milk line d) Ipsilateral nodes or internal mammary nodes are the most common route of metastasis e) Hormone actions on breast i) Estrogen: growth of adipose tissue and lactiferous ducts ii) Progesterone: lobular growth and alveolar budding 2) Physical examination a) The best time to perform a breast exam is in the follicular phase o f the menstrual cycle 3) Diagnostic Testing a) Mammography i) Screening and diagnostic ii) Indications of malignancy: microcalcifications, distortion of the normal architecture, discrete non-palpable lesion iii) Able to detect lesions two years before they become palpable b) Ultrasound i) Differentiate between solid and cystic masses ii) Preferred method of evaluation in women < 40 years old c) MRI: more often used as an adjunct to diagnosis, and for early detection in high risk patients d) Fine Needle Aspiration Biopsy i) Clear fluid -> simple cyst F/U in 4-6 months ii) Bloody fuild -> path lab, mammogram, and or US e) Core Needle Biopsy i) Biopsy solid masses f) Page 287; Figure 31.5 4) Benign Breast Disease a) Mastalgia i) Cyclic mastalgia: begins in the luteal phase and is resolved with menses, bilateral, and involves the outer quadrant of the breast ii) Non-cyclic mastalgia: tumors, mastitis, cysts, or history of breast surgery iii) Non-mammary pain: musculoskeletal pain ObGyn Beckman 61 ObGyn Chapter 31: Disorders of the Breast

iv) Treatment: Danazol, bromocriptine, GnRH analogs, tamoxifen, OCP (cyclic mastalgia) b) Nipple Discharge i) Ductal ectasia: fibrocystic changes of the breast leading to non-bloody, non-spontaneous, bilaterally nipple discharge. ii) Milky discharge: pregnancy, endocrinologic, or medications iii) Purulent discharge: underlying infection iv) Bloody unilateral discharge: carcinoma (usually ductal and requires ductography and ductal excision c) Breast masses i) Non-proliferative (1) Fibrocystic: dilation and formation of cyst within a lobule (2) Adenosis: increase in the number of glands (3) Simple fibroadenoma: solid, round, rubbery, and mobile; respond to pegnancy hormones and enlarge ii) Proliferative without atypia (1) Epithelial hyperplasia, sclerosing adenosis -> radial scar (form of sclerosing adenosis) intraductal papillomas (may produce a serosanguinous discharge) (2) 1.5 -2.0x risk for malignant transformation iii) Proliferative with atypia (1) DCIS (a) Strong likelihood of transforming into invasive cancer (2) LCIS (a) More likely to transform into atypical lobular hyperplasia (3) Management (a) Excisional biopsy (core needle/surgical) (b) Estrogen modulator (tamoxifen) to reduce the risk of invasive breast cancer (4) 8-10x risk of malignant transformation 5) Breast Cancer a) Risk factors i) Age is the single largest risk factor for developing breast cancer ii) Caucasion iii) First degree relative with breast cancer (breast cancer before 40 evaluate for BRCA mutation) iv) BRCA1 and BRCA2 v) Early menarch, late menopause, delayed childbearing or nullparity vi) Radiation, EtOH, and obesity vii) Gail method: risk assessment tool (1) High risk women (5 year risk of 1.7% may consider prophylatic therapy) -> medical: tamoxifen/raloxifene; surgical: mastectomy b) Histologic types: ductal (invasive ductal being the most common type), lobular, and nipple c) Staging i) TNM system along with Her2/neu (+ equals a negative prognosis) and ObGyn Beckman 62

Erb2 receptors (+ equals a positive prognosis) d) Treatment i) Surgical -> lumpectomy or mastectomy (radical mastectomy also takes the axillary lymph nodes) ii) Radiation therapy is added for advanced disease and conservative lumpectomies iii) Adjucvent (systemic) therapy: takes place irregardless of the staging -> chemotherapeutic and hormonal therapies iv) Trastuzumab -> acts on breast cancers that are Her2/neu positive e) Management: First two years F/U every 3-6 months and then annually after that f) Prevention i) Breast self examination ii) Mammogram (value increases with age) ObGyn Chapter 32: Gynecologic Procedures 1) Ultrasonography a) Safe for both pregnant and non-pregnant patients b) Different dimensional US allows for different analysis i) 3D: mullerian abnormalities ii) 4D: movement c) Probes i) Transabdominal (1) Increase depth used for large uterine and adnexal masses (2) Problematic with obese patients ii) Transvaginal (1) Cervix, uterus, fallopian tubes, or ovaries (2) Shorter depth of penetration improving clarity d) Most valuable gynecologic imaging for masses i) Differentiate between cystic and solid adnexal masses ii) Determine leiomyoma size and number e) Endometrial thickness detected as less than 5mm is abnormal in postmenopausal women and needs to be evaluated for endometrial carcinoma f) Sonohysterography i) Identify intrauterine polyps/submucosal leiomyomas ii) Main role in diagnosing abnormal uterine bleeding 2) Computed Axial Tomography a) Not to be used in pregnancy 3) MRI a) Assessment of lesions in the breast and staging of cervical cancer 4) Breast Imaging a) Mammography: used to detect breast tumors, but has a high false positive rate 5) Hysterosalpingography a) Uses ObGyn Beckman 63

i) Fallopian patency (infertile women) ii) Uterine abnormalities b) Radio-opaque dye is added to the uterus if the dye reaches the peritoneum then the fallopian tubes are patent 6) Gynecologic Procedures a) Genital Tract Biopsy i) Vulva, vagina, cervix, and endometrium (1) Circular punch biopsy 7) Colposcopy a) Uses: to evaluate an abnormal pap smear b) May also use a cone biopsy to evaluate an abnormal pap smear 8) Cryotherapy a) Uses: to destroy cervical intraepithelial neoplasia and condlyoma acumata b) MOA: create water crystals in the cells 9) Laser Vaporization a) Uses: vaginal and vulvar intraepithelial neoplasia, condyloma 10) Dilation and Curretage a) Indications i) AUB, incomplete/missed abortion, difficult EMB, postmenopausal bleeding, and suspected endometrial polyps 11) Endometrial Ablation a) Treatment of AUB in women who do not wish to become pregnant b) NOTE: not a method of sterilization 12) Pregnancy termination a) Dilate the cervix and either flush the uterine cavity (first trimester) or grasp with forceps (second trimester b) None surgical options i) Mifepristine and misoprostol ii) Methotrexate and misoprostol 13) Hysterectomy a) Total: takes all of the uterus b) Subtotal/Super cervical: takes the uterine corpus, leaving the cervix c) NOTE:does not include the taking of the fallopian tubes or the ovaries d) Types: i) Abdominal hysterectomy ii) Vaginal hysterectomy iii) Laproscopic assisted hysterectomy iv) Total Laproscopic hysterectomy ObGyn Chapter 33: Reproductive Cycles 1) Introduction a) Average years of the reproductive cycle 15 45 yo b) Menstrual cycle (average 28 days; 23-35 day range) i) Follicular phase: begins with onset of menses and ends with LH surge ii) Ovulation: 30-36 hours post LH surge ObGyn Beckman 64

iii) Luteal phase: begins on the day of the LH surge and ends with the onset of menses iv) NOTE: follicular phase duration can vary, but the luteal phase is approximately 14 days 2) Hypothalamic-Pituitary-Ovarian Axis a) Hypothalamus: i) GnRH pulsatile release to the anterior pituitary stimulating the release of FSH and LH b) Pituitary: i) FSH initially secreted at a higher rate first due to hypoestrogen state of the beginning of the cycle. However, estradiols, produced by the ovary in response to FSH will feedback inhibit FSH release and increase LH release. c) Ovary: i) LH surge which ruptures the follicle and converts it the corpus luteum ii) The corpus luteum under the influence of LH will begin to secrete progesterone iii) Follicular phase (1) Granulosa cells: produce estradiol from androgen precursors (2) Theca cells: derived from the ovarian stroma, and produce androgens to feed to the granulosa cells iv) Luteal phase (1) Granulose theca cells are converted into the corpus luteum and produce progesterone via stimulation by LH 3) Reproductive Cycle

a)

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4) 5) 6) 7)

b) Phase I: menstruation and follicular phase (endometrial proliverative) i) Endometrium: withdrawal of progesterone (primarily) and estrogen leads to shedding of the endometrium (1) Prostaglandin in the secretory endometrium stimulates uterine contraction (cramps) c) Phase II: Ovulation i) Meisosis is halted at metaphse II and the remains there until fertilization ii) Mittelschmetz: twinge of pain at the time of ovulation d) Phase III: Luteal phase (endometrial secretory phase) i) Switch in hormone production from estrogen to progesterone ii) Progesterone inhibits FSH and LH release iii) Lack of fertilization causes involution of the corpus luteum and sharp decrease in progesterone -> releases FSH from inhibition and levels begin to rise iv) Pregnancy hCG and LH analog continues support of the corpus luteum production of progesterone until the placenta can take over v) Corpus albicans -> scar from involuted corpus luteum Endometrium a) AUB: lack of progesterone withdrawal -> over proliferation phase causing necrotic tissue and irregular bleeding -> most often due to anovulatory cycles Endocervix a) Estrogen: thin watery mucous production -> facilitates sperm transport b) Progesterone: decreases the secretion of cervic mucous Breasts a) Estrogen: influences enlargement in puberty b) Progesterone: breast tenderness and fullness Hypothalamic Thermoregulation Center a) Progesterone: thermogenic effects and shifts the basal body temperature (most accurate documentation taken in the morning) up 0.5-1.0 degrees C ObGyn Chapter 34: Puberty

1) Introduction a) Secondary sexual development: thelarche, pubarche, menarche, and ovulation 2) Abnormalities of Pubertal Development a) Initial evaluation: measurement of FSH and LH to distinguish location of the disorder b) Precocious puberty i) True (central) ->GnRH depenent (1) Idiopathic, tumor, infection (2) Arcuate nucleus in the hypothalamus is prematurely activated (3) Elevated estrogen -> premature closure of the epiphyseal plates resulting in short stature ii) Precosious psuedohypertrophy -> GnRH independent (1) Cysts or tumors -> secrete androgens/estrogens ObGyn Beckman 66

(2) McCune-Albright syndrome (a) Polyostotic fibrous dysplasia -> multiple bone fractures, caf-aulait spots and precocious puberty (b) Estrogen production autonomous from FSH stimulation (3) Congenital adrenal hyperplasia (a) 21/11-hydroxylase deficiency (b) Increase production of androgens due to the inability to produce glucocorticoids to feedback inhibit ACTH secretion (c) Treatment GnRH agonist iii) Drugs c) Delayed Puberty i) No secondary sex characteristics by age 13, no evidence of menarche by age 15, or when menses have not begun 5 years after thelarche (1) Hypergonadotropic hypogonadism -> Turners syndrome (a) Treatment: is exogenous hormones administered similar to how they are endogenously made (2) Hypogonadotropic hypogonadism (a) GnRH is not produced (b) Physiologic, Kallman syndrome (olfactory system is not developed and the arcuate nucleus does not secrete GnRH), anorexia, pituitary dysfunction (craniophyrangioma -> + calcifications), hyperprolactinemia, and drug use (3) Anatomical (a) Mullerian agenesis (normal secondary sex characteristics, but no tubes or uterus (b) Imperforate hymen: obstruction (c) Transverse vaginal septum: obstruction ObGyn Chapter 35: Amenorrhea and AUB 1) Amenorrhea a) Primary amenorrhea: never had menstruated b) Secondary amenorrhea: menstruating women who hasnt menstruated for 36 months c) Etiology i) Pregnancy ii) Hypothalamic Pituitary dysfunction (1) Lack of GnRH pulsing or GnRH release (2) Changes in weight, drug induced, neoplasms (prolactinoma, craniopharyngioma), psychogenic, trauma, or chronic illnesses (3) Management -> differentiate between hypothalamus or pituitary iii) Ovarian dysfunction iv) Alteration of the Genital Outflow tract (1) Primary amenorrhea -> congenital (2) Secondary amenorrhea: asherman syndrome, S/P D and C d) Treatment ObGyn Beckman 67

i) Progesterone challenge test (1) Bleeding occurs -> anovulatory cycle/oligo-oluvatory (2) No withdrawal bleeding -> hypoestrogen/outflow obstruction ii) Prolactin levels (1) Elevated prolactin levels -> prolactinoma, primary hypothyroidism, drugs iii) Induce ovulation (1) Clomiphene, GnRH agonist, or aromatase inhibitors 2) Abnormal Uterine Bleeding a) Anovulatory uterine bleeding -> PCOS, exogenous obesity, and adrenal hyperplasia b) Anovulation -> irregular bleeding because the body has not progesterone withdraw to have a regular cycle, instead shedding occurs with as the endometrium becomes necrotic and sheds off c) Luteal phase defect: ovulation occurs, but the corpus luteum fails to form d) Mid-cycle bleeding: abrupt drop in estrogen after ovulation e) Diagnosis i) AUB is a diagnosis of exclusion of anatomic and neoplastic causes ii) Test for ovulation -> predictor kit, or basal body temperature iii) Endometrial biopsy -> anovulation/AUB elevated estrogen leading to endometrial hyperplasia and cancer f) Treatment i) Progesterone supplementation to mimic a normal menstrual cycle ii) OCP iii) Heavy bleeding (1) Short term course -> high dose estrogen and progesterone (2) Long term: progesterone supplementation or OCP iv) Unresponsive to medical treatment considered endometrial ablation/hysterectomy ObGyn Chapter 36: Hirsutism and Virilization 1) Introduction a) Hirsutism: excess terminal hair pattern in a male pattern b) Virilization:masculinization of a women and associated with marked increase in circulating testosterone i) Enlargement of the clitoris, temporal balding, and deepening of the voice c) Etiology: idiopathic, PCOS, or CAH 2) Androgen Production and Action a) Produced in the adrenal glands, ovaries, and adipose b) Androgens i) DHEA: secreted in the adrenal glands ii) Androstenedione: secreted in the adrenal glands and ovaries (theca cells) iii) Testosterone: secreted adrenal glands, ovaries (theca cells), and adipose (1) Androstenediones is converted in adipose tissue to form testosterone iv) DHT: converted from testosterone and in the periphery by 5-reductase ObGyn Beckman 68

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c) Most testosterone in the female is bound to sex hormone-binding globulin (SHBG) i) Estrogen stimulates SHBG production in the liver PCOS a) Most common cause of androgen excess and hirsutism b) Clinical Presentation: oligomenorrhea/amenorrhea, acne, hirsutism, and infertility, obesity, ancanthosis nigricans c) Hormones: i) Increase in the LH:FSH ratio ii) Estrone > estradiol iii) Androstenedione at the upper limits of normal or increased iv) Testosterone at the upper limits of normal or increased d) Hyperestrogen and hyperandrogen state e) Metabolic syndrome: 2 or 3 of the following i) Type II DM, lipid abnormalities, HTN, and cardiovascular disease f) Treatment i) OCP, weight reduction, metformin and clomiphene g) Hyperthecosis: severe type of PCOS may be refractory to OCP therapy Ovarian Neoplasms a) Sertoli-Leydig cell tumors i) Unilateral, and secretes testosterone ii) Rapid onset of hirsutism, acne, and virilizatoin iii) Two stages -> 1) loss of feminity 2) gain of masculinity iv) Labs (1) Low FSH, LH, and androstenedione elevated testosterone b) Gynadroblastoma: granulosa and atthrenoblastoma componenets; masculinization, endometrial hyperplasia, and irregular uterine bleeding c) Lipid (lipoid) cell tumor: sheets of round, clear, pale-stainging cells; masculinization of the female and elevated 17-ketosteroids d) Hilar cell tumors: overgrowth of mature hilar cells from the ovarian mesenchyme i) Histological: Rienke albuminoid crystals Congenital Adrenal Hyperplasia a) 21-hydroxylase deficiency i) Accumulation of progesterone and 17-hydroxyprogesterone which are subsequently metabolized subsequently to DHEA ii) Disease ranges from virilization/life-threatening salt wasting disease to terminal body hair, acne, subtle alterations in menstrual cycles iii) History: pubarche before thelarche iv) Diagnosis: elevated 17-OH progesterone, DHEA, and androstenedione v) Mineral corticoids decreased, sex steroids increased b) 11-hydroxylase i) Similar symptoms, but milder ii) Mineral corticoids increased, sex steroids increased iii) Sodium retention and HTN Cushing Syndrome: Excess cortisol (adrenal tumor or elevated ACTH) ObGyn Beckman 69

7) Adrenal Neoplasm a) CP: elevated DHEA and tumor on CT or MRI 8) Constitutional Hirsutism a) Diagnosis of exclusion b) Women with an increase activity of 5 reductase c) Treatment: i) Spironolactone: adrogen antagonist and 5 reductase inhibitor ii) Flutamide: androgen blockade iii) Finasteride: 5 reductase inhibitor (need to be placed on OCP due to teratogenic effects) 9) Iatrogenic Androgen Excess a) Danazol, progestin containing OCP ObGyn Chapter 37: Menopause 1) Introduction a) Menopause: permanent cessation of menses after cessation of estrogen production b) Perimenopause: is the period just before menopause c) Climacteric: describes the time period during which the changes of menopause occurs 2) Menstruation and Menopause a) Estradiol is the major estrogen of premenopausal ovaries b) Advance age remaining oocytes become resistant FSH -> increase in FSH several years before menopause c) Menopause usually occurs around the age of 50 -52 i) If menopause occurs before the age of 40 it is considered premature ovarian failure d) Post-menopause hormones i) LH continues to stimulate the production of testosterone ii) Estrone becomes the predominant estrogen (extragonadal estrogen) (1) Concentration is directly related to body fat due to the conversion of androstenedione to estrone in fatty tissue 3) Signs and Symptoms of menopause a) Menstrual cycle alterations: increase in anovulatory cycles (13-14/year to 34/year) b) Hot Flushes and Vasomotor instability: decreased estrogen which leads to vasomotor instability -> first symptom of perimenopause c) Sleep disturbances: increase in the latent phase and decrease in restful sleep d) Vaginal Dryness and Genital Tract Atrophy i) Atrophy occurs due to decrease in growth stimulation from estrogen ii) Atrophic vaginitis: itching and burning with vaginal atrophy -> may treat with topical hormones iii) Decrease in estrogen with a history of childbearing causes cystocele and rectocele (loss of support for the bladder and rectum) iv) Atrophic urethritis ObGyn Beckman 70

e) Mood changes, skin thinning, increase facial hair, thinning of the nails f) Osteoporosis i) Bone Demineralization -> accelerated in cases of hypoestrogen states ii) Estrogen has a permissive effect on osteoblast activity and has a great effect on trabecular bone iii) Prevention: calcium supplements, weight bearing exercises, +/- estrogen therapy, vitamin D supplements, osteoclast inhibitors (biphosphonates: aldronate/ibandronate), SERM (raloxifene: inhibits bone resorption and turnover) iv) DEXA-S test for bone mineralization g) Cardiovascular Lipid Changes i) Increase in total cholesterol and LDL, decrease in HDL 4) Premature Ovarian Failure a) Symptoms: hot flushes, hypoestrogen states, and secondary amenorrhea (infertility) b) Diagnosis is confirm by elevation of FSH c) Etiology i) Genetic: partial loss of the long arm of the X chromosome (total loss -> Turners) ii) Savage Syndrome (Gonadotropin-Resistant Ovary Syndrome) (1) Follicles are resistant to FSH and LH (2) Pregnancy has been achieved with estrogen supplementation increasing follicle sensitivity to FSH iii) Autoimmune: autoantibody against ovarian endocrine tissue iv) Smoking, alkylating chemotherapy, and hysterectomy 5) Management of Menopause a) Estrogen therapy with complement progesterone therapy to prevent endometrial hyperplasia/carcinoma i) Complications: CVD, thromboembolic disease, increase risk of breast and endometrial cnacer ii) Decrease risk of ovarian and cancer, Decrease in hip fractures iii) Should only be used for short term relief and is most effective in the early stages of menopause (1) Heart healthy lifestyle changes (2) Soy, isoflavones, St. Johns wort, and black cohosh may provide shortterm relief, but are not FDA approved or regulated natural does not mean safe. ObGyn Chapter 38: Infertility 1) Introduction a) Infertility: has not conceived a child in 12 months of trying b) Fecundabilituy: probability of achieving a pregnancy in a given menstrual cycle c) Fecundity: probability of achieving a live birth

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d) 50% of those who have not conceived in the first year will conceive a child within in 36 months 2) Evalation of Infertility a) Due to decline in fecundity in older women evaluation may take place before 12 months for fertility b) Ovulation i) Basal body temperature (1) Ovulation occurs one day prior increase in basal body temperature ii) Urine LH kits (1) After increase in LH (LH surge) ovulation occurs about 24 hours later iii) Oligo-ovulation/anovulation (1) Pregnancy, hypothyroidism, ovarian failure, PCOS, hyperprolactinemia -> Pregnancy test, serum T4, FSH, estrogen, and prolactin c) Anatomic Factors i) Uterus: more often associated with early loss of pregnancy than infertility, but can still be evaluated -> hysterosalpingography/US ii) Fallopian tubes (1) Fertilization occurs in the ampulla (2) Hysterosalpingography/laparoscopy iii) Failure of dye injected in the fallopian tube to reach the peritoneum is evidence of obstruction (i.e. pelvic adhesions) iv) Evaluation: hysterosalpingography/US -> hysterscope -> laparoscope (at this stage you can remove adhesions and endometriosis 3) Male Infertility a) Semen analysis i) Sample is from 2-3 days of abstinence ii) Quantity and quality of seminal fluid; sperm concentation, motility, and morphology iii) May be problems with sperm cervical mucous interaction (1) IVF and intrauterine insemination bypass any abnormalities of the sperm and cervical mucous iv) Requires two samples to verify abnormal findings -> may be indicative of a testicular or pituitary tumor v) Etiologies semen dysfunction (1) Primary/secondary hypogonadism -> FSH and LH levels (2) Elevated prolactin (prolactinoma) (3) Azoospermia -> CF or Kleinfelters (4) Obstruction: collect sperm before the obstruction (epididymis) to obtain motile and healthy sperm -> IVF 4) Treatment a) Laparoscope: to correct obstructions or uterine abnormalities (lieomyomas, endometrial polyps, intrauterine adhesions, etc.) b) Ovulation stimulation i) Clomiphene citriate -> antiestrogen stimulating gonadotropin release; complications is multiple gestation ObGyn Beckman 72

ii) Urine LH kit to determine ovulation and then have intercourse or intrauterine insemination iii) TVUS to see follicle and time ovulation for proper time of intercourse iv) Controlled Ovarian hyperstimulation (gonadotropins): for people who fail clomiphehe: monitor follicle growth to time intercourse (1) Complication: hyperstimulation syndrome c) Intrauterine insemination i) Take semen, clean it up to only have sperm (want about 1 million), then inject into the uterus at the time of ovulation d) Assisted Reproductive Technologies i) IVF: ovarian stimulation to mature multiple oocytes, oocytes are removed, in vitro insemination, transfer of embryos into uterus (1) Ovarian stimulation GnRH analog and hCG prior to retrieval for final maturation ii) After oocyte retrieval progesterone must be supplemented to favor implantation ObGyn Chapter 41: Gestational Trophoblastic Neoplasia 1) Introduction a) Gestational trophoblastic neoplasia i) Benign disease called a hydatidiform mole (molar preganancy) ii) Persistent mole is considered a gestational trophoblastic disease (malignant) and is treated with chemotherapy iii) Clinical features (1) Presentation of pregnancy (2) Diagnosis is by US (3) Tumor marker is beta hCG 2) Epidemiology a) Highest incidence is in Asians b) Associated with low diet intake of carotene/ vitamin A consumption 3) Hydatidiform Mole a) Replacement of normal placental trophoblastic tissue by hydropic placental villi b) Complete mole: has no identifiable embryonic or fetal structures i) Blighted ovum + dizygotic sperm ii) Blighted ovum + two monozygotic sperm iii) More common than partial moles and are more likely to undergo malignant transformation c) Partial mole: identifiable fetal/embryonic parts i) Triploidy ii) Monozygotic ovum + dizygotic sperm iii) Monozygotic ovum + two monozygotic sperm 4) Clinical Presentation a) First trimester: diagnosed by US -> snowstorm appearance +/- fetal parts (partial/complete respectively) ObGyn Beckman 73

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b) Second trimester: painless vaginal bleeding c) Abnormally high beta hCG and uterus larger than expected for gestation age i) Marked gestational HTN, proteinuria, and hyperthyroidism ii) Sever HTN before 20 weeks -> must consider HTN iii) Theca-lutein cyst develop from beta hCG stimulation d) Invasive mole: histologically identifiable to a complete mole i) invades the myometrium and surrounding structures -> beta hCG levels do not fall after evacuation and leads to GTD e) Partial mole i) Present as a missed abortion ii) Uterine growth < expected for the gestational age Treatment a) D and C (suction curettage followed by gentle sharp curettage) b) The larger the uterus the greater the risk of pulmonary complications: trophoblastic emboli, fluid overload, and anemia c) Theca lutein cyst usually regress with removal of the molar pregnancy and decrease in beta hCG levels d) Those wishing no longer to have children may elect for hysterectomy, but the risk of neoplasm transformation is still present Postevacutaion Management a) Rh negative moms should be given Rhogam b) Follow up visit for 6-12 months i) Pelvic exam ii) Monitor decrease in beta hCG (1) 48 hours post evacuation, 1-2 weeks while still elevated, and 1-2 months after decrease back to baseline c) OCP or other form of contraception to prevent pregnancy Malignant gestational trophablastic neoplasia a) Postmolar or persistent GTD b) Choriocarcinoma -> red granular appearance intermingled with syncytiotrophoblast and cytotrophoblast c) Myometrial involvement and hematogenous distant mets (lungs and brain most common) d) May follow molar pregnancy, normal pregnancy, abortion, or ectopic pregnancy e) Should be considered in AUB 6 weeks post pregnancy f) Treatment i) Non-metatstatic (1) Methotrexate & actinomycin D ii) Metastatic (1) Etoposide, methotrexate, actinomycin D, cyclophosphamide, oncovin (vincristine) (2) +/- radiotherapy Placental Tumors a) Trophoblastic disease: monomorphic populations of intermediate cytotrophoblast that are locally invasive at the placental implantation site ObGyn Beckman 74

b) Secretes small amount of beta hCG and is better followed by hPL (human placental lactogen) c) Rare to have mets and responds well to chemotherapy ObGyn Chapter 42: Vulvar and Vaginal Disease and Neoplasia 1) Introduction a) Major symptoms: pruritus, burning, non-specific irritation, and/or appreciation of a mass b) Diagnostic methods should always include a good history, inspection, and biopsy i) Punch biopsies ii) Colposcopy: evaluate vulvar atypia and intraepithelial neoplasia 2) Benign vulvular disease a) Lichen sclerosus i) CP: (1) Vulvar pruiritus (2) Location is diffuse and bilateral -> whitish epithelium (onion skin), skin appears as cigarette paper/ parchment paper (3) Loss of anatomical structure and may result in severe stenosis of the vaginal intoitus ii) Etiology: unkonwn, but has a familial link (1) Considered an inflammatory process (prostaglandins/leukotrienes) because it does respond to topical steroids iii) Histology: band of lymphocytic infiltrate, hyperkeratosis -> flattening of the rete pegs (acanthosis) iv) Treatment: topical steroids (clobetasol) v) No increase risk of developing cancer b) Lichen Simplex Chronicus i) The itch that generates a rash -> mechanical irritation which leads to hyperplasia and lymphocytic infiltration ii) CP: vulvar pruritus and or burning iii) PE: erythemic areas with hyperpigmented plaques of red to reddish brown iv) Treatment: (1) Antipruritic medications: benapdryl/hydroxyzine hydrochloride (atarax) (2) Topical steroid (3) If it last longer than three months then a vulvar biopsy is warranted c) Lichen Planus i) Desquamtive lesion: thinning of the epithelium, loss of rete pegs, and lymphocytic infiltrate ii) CP: itching, burning, dyspareunia, profuse vaginal discharge iii) PE:Lacey white appearance with a patchy red background iv) Tx: topical steroids d) Psoriasis: ObGyn Beckman 75

i) AD inheritance ii) Appearance: slightly raised round/ovoid lesions with a silver scale appearance (1) Ausptiz sign (2) Acanthosis iii) Tx: Topical corticosteroids e) Vulvar Dermatitis i) Histology: spongiotic pattern characterized by epidermal edema ii) Eczema: (1) Exogenous form -> irritant/allergic contact dermatitis (a) Reaction to irritants (2) Endogenous -> atopic dermatitis iii) Seborrheic dermatitis: chronic irritation of the sebaceous glands (1) Lesions are pale red to yellow/pink; oilly appearing crust (2) Diagnosis is usually based on the knowledge of SD elsewhere (3) Histology: spongiotic and acanthotic iv) Tx: removal of the offending agent, perineal hygiene (aluminum acetate), topical corticosteroid, and antipruritic agents f) Vestibulitis: i) Inflammation of the vestibular glands that lie around the hymen ii) CP: insertional dyspareunia, pain on insertion of tampon iii) PE: includes careful inspection of the area between the labia minora and the hymen and can be elicited iv) Tx: topical corticosteroids, topical lidocaine, surgical excision (1) Other treatments include low dose TCA, fluoxetine, calcium citrate (remove oxalic acid xtals) g) Vulvar Lesions i) Sebaceous (inclusion cysts): inflammatory of sebaceous glands ii) Cyst of the canal of Nuck (hydrocele): fluid accumulation around the round ligament in the labia majora iii) Fibromas: proliferation of smooth muscle of the vuvla and vagina (easily excised) iv) Hidradenoma: inflammation of the eccrine sweat glands 3) Vulvar Intraepithelial Neoplasia a) VIN 1 i) Mild dysplasia that demonstrates minimal to mild squamos atypia limited to the lower epidermis ii) Occurs with condylomata acuminata iii) Biopsy and excision iv) Has not been related to carcinoma transformation b) VIN usual (VIN 1 and 2) i) High grade, HPV related lesions ii) Has been linked to carcinoma transformation iii) Risk factors (1) Strong link to CIN (2) Smoking ObGyn Beckman 76

iv) CP: chronic irritation with a raised mass lesion v) PE: acetic acid to identify lesions vi) Subtypes: warty, basaloid, or mixed vii) Cell types have atypia, nuclear pleomorphism, and loss of differentiation viii) Tx: corticosteroids, 5-FU, and imidazoquinolone ix) May be adjacent to squamos cell carcinoma c) VIN differentiated type i) VIN carcinoma in situ ii) Not HPV related, related to SCC or lichen sclerosis 4) Paget Disease a) Gross appearance: fiery red background with mottled whitish hyperkeratotic areas b) Histology: large, pale cells of apocrine origin below the surface epithelium c) Increase in skin, colon, or breast cancer d) Tx: wide local excision or simple vulvectomy 5) Vulvar Cancer a) 90% are squamos cell carcinomas -> 2% melanoma -> sarcoma b) Most commonly presents in post menopause women with a chief complaint of vulvar pruritus c) SCC i) Progression: remains local for some time and then metastasizes to the lymph nodes ii) Surgical staging iii) Treatment: (1) Surgical: conservative measures to radical vulvectomy (2) Medical: radiation and chemotherapy iv) Prognosis (1) 5 year survival rate stage I and II 60-80%; stage III 45%; stage IV 15% d) Melanoma i) CP: raised, pruritic, pigmented lesion ii) Survival is based on the depth of invasion e) Carcinoma of the Bartholin Gland i) Tx: radical vulvectomy and bilateral lymhadenectomy 6) Vaginal Disease a) Vaginal neoplasias are rare and are usually secondary to cervical or vuvlar cancers that spread to the vagina b) Benign i) Gartner duct cyst: vestigial remnants of the mesonephric or wolffian ducts ii) Inclusion cyst: imperfect approximation of the episiotomy that may be excised if symptomatic c) VAIN i) 1: basal epithelial layers ii) 2: up to two thirds of the vaginal epithelium iii) 3: involves most of the vaginal epithelium

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iv) Tx VAIN I and II: monitored, may not require treatment, and related to HPV v) Diagnosis: colposcopy with directed biopsy is the definitive method of diagnosis vi) Tx VAIN III: excision and 5-FU d) Vaginal cancer i) Adenocarcinoma and vaginal melanoma ii) Nonsurgical staging iii) Tx: hysterectomy, upper vaginectomy, and pelvic lymphadenectomy e) Sarcoma botryoides (embryonal rhabdomyosarcoma) i) Grape like polyps protruding from the introitus in the pediatric age ObGyn Chapter 43: Cervical Neoplasia and Carcinoma 1) Cervical Intraepthithelial Neoplasia a) Etiology i) HPV 16, 18, 31, and 45 -> cervical cancer ii) HPV 6 and 11 -> condylomata acuminata and LSIL iii) Histology of the cervix (1) Prepubertal: ectocervix -> squamos; endocervix -> columnar epithelium (2) Where the squamos and columnar epithelium meet is called the squamocolumnar junction and is the where 90% of cancers occurr (3) Post-puberty: part of the endocervix everts and due to the hostile environment of the vagina the columnar epithelium changes to squamos forming the transformation zone (4) Nabothian cysts: glands of the cervix during metaplasia become trapped in squamos epthithelium. iv) HPV: is a DNA virus that is incorporated into the host DNA, and if it is the correct regulatory spot may transform the cells into intraepithelial lesions/cancer v) Koilocytosis: virion particles within the cell producing damage b) Risk Factors i) Immunodeficiency, Not leading a conservative sexual lifestyle, cigarette smoking, and immunodeficiency c) Classification i) Squamos (1) ASC, LSIL (CIN 1), HSIL (2) ASC-US, ASC-H ii) Glandular (1) AGC, endocervical adenocarcinoma in situ (AIS), d) Evaluation of abnormal pap smears i) Colposcopy and biopsy: direct visualization of the cervix and requires visualization of the entire SCJ to be considered satisfactory ii) Evaluate the cervical canal can be done by endocervical curretage or cervical conization ObGyn Beckman 78

iii) HPV DNA: used as a triage tool for women e) Management guidelines: Figure 43.3 43.6 p. 381-383 f) Treatment i) Ablative methods: Cryotherapy (freeze-thaw cycles): used mostly for CIN 1 ii) Excisional methods: Cone biopsy (more appropiate for AGC) or LEEP (thermal damage to borders) iii) If the margins are not clean than repeat conization or close follow-up 2) Cervical Carcinoma a) CIN precedes cervical carcinoma b) Etiology is HPV in more than 90% of the cases c) Symptoms: intermittent spotting, post-coital bleeding, dyspaurenia d) Spreads by direct invasion or by lymphatics e) Staging is clinical (Box 43.3) f) Treatment i) Stage Ia1: conization or hysterectomy ii) Stage Ia2: radical hysterectomy with lymph node dissection or radiation iii) Stage IIa: radical TAH and lymph node dissection iv) Stage IIb and above: radiation g) Complications of radiation therapy: i) Radiation cystitis or proctitis, intestinal/vaginal fistulae, hemorrhagic proctitis or cystitis h) F/U: i) First two years: 3 times/year ii) Years 3-5: two times/year iii) Pap test and chest x-ray annually 3) Cervical Cancer Prevention a) Pap test, HPV vaccine, and practicing safe sex

ObGyn Chapter 44: Uterine Leiomyoma and Neoplasia 1) Leiomyomata a) Localized proliferation of smooth muscle cells surrounded by a pseudocapsule of compressed muscle fibers b) Most common indication for a hysterectomy c) Types: i) Intramural: within the muscular wall of the uterus ii) Subserosal: below the serosal layer iii) Submucosal: below the endometrium iv) Pedunculated: appears on stump like structures d) Hormonally responsive (progesterone: may stimulate growth) 2) Leiomyosarcoma a) Development of new neoplasm

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b) Sx: posmetnopausal bleeding, unusual vaginal discharge, abdominal mass, and pelvic pain Symptoms a) Menorrhagia i) Alteration of myometrium contraction forces, impairment of overlying endometrium hormonal response, and pressure necrosis ii) Most commonly associated with sumbucosal/intramural leiomyomas b) Pelvic pressure i) Pressure to the ureters -> hydroureter/hydronephrosis c) Dysmenorrhea Diagnosis a) Physical examination: large, midline, irregular mass b) Imaging studies: US -> acoustic shadowing c) DO NOT use endometrial biopsy d) Hysteroscopy: evaluation of submucosal fibroids e) All else fails try surgical evaluation Treatment a) Mild disease -> reassurance and observation b) OCP and NSAIDS c) Myomectomy: to retain fertility d) Hysterectomy e) Medical treatment i) GnRH analogs to suppress cyclic hormones -> reduce fibroid and blood loss ii) Danozol: reduces release of endogenous estrogen f) MRI guided focused ultrasound Effect of leiomyomata on pregnancy a) Become a problem when the myoma is greater than 3 cm. b) Respond to hormones of pregnancy and may outgrow their blood supply causing red or carneous degeneration c) Increase risk of preterm labor, placental abruption, pelvic pain, and CS ObGyn Chapter 45: Cancer of the Uterine Corpus

1) Introduction a) Two types: endometrial carcinoma or sarcoma b) Endometrial carcinoma is the most common genital tract malignancy 2) Endometrial Hyperplasia a) Simple hyperplasia: hyperplasia of both glands and stroma b) Complex hyperplasia: primarily glandular hyperplasia c) +/- atypia d) Pathophysiology and Risk Factors i) Unopposed estrogen exposure (endogenous or exogenous) ii) Obesity, nullparity, infertility, early menarche, late menopause, HTN, DM iii) Past history of tamoxifen exposure (breast estrogen antagonist; endometrium estrogen agonist) ObGyn Beckman 80

iv) BRCA1, BRCA2, HNPCC e) AUB is the hallmark symptom for endometrial hyperplasia f) Evaluation i) Endometrial biopsy ii) If cellular atypia is observed and D and C/hysteroscopy should be next step iii) +/- transvaginal biopsy (1) >5mm indicative of hyperplasia (2) <5mm does not rule out hyperplasia just makes it less likely g) Management i) Endometrial hyperplasia without atypia -> progesterone therapy ii) Endometrial hyperplasia with atype (1) D and C to gain a better sample of the endometrium to rule out cancer (2) Preserve fertility: high dose progesterone (3) Hysterectomy 3) Endometrial Polyps a) Very similar to the endometrial hyperplasia just more focused into polyp 4) Endometrial Carcinoma a) Forms: i) Adenocarcinoma (most common), adenocanthoma (benign squamos), adenosquamos carcinoma(malignant squamos) ii) Clear cell carcinoma, papillary serous adenocarcinoma (psammoma bodies) b) Types i) Type 1: estrogen dependent, less severe ii) Type 2: estrogen independent more severe c) Diagnosis i) Post-menopausal bleeding with a confirmatory endometrial; biopsy ii) Elevated CA-125 indicative of advanced disease d) Staging i) Endometrium only ii) Extended to the cervix iii) Pelvic walls and lymph nodes iv) Pelvic cavity and distant mets e) Treatment: i) Stage I/II (1) Preserve fertility: high dose progesterone (2) RAH-BSO ii) Stage III/IV (1) RAH-BSO and radiation (decrease risk of recurrence) f) Recurrent endometrial cancer i) There is not much left to do. May try high dose progestin or chemotherapy (cisplatin, doxorubicin, or paclitaxel), but this only provides short term remission. Longterm survival is unlikely. 5) Uterine Sarcoma a) Reference Chapter 44, leiomyosarcoma ObGyn Beckman 81

ObGyn Chapter 46: Ovarian and Adnexal Disease 1) Differential Diangnosis a) Renal/Urologic i) Upper and lower UTI, renal/ureter caliculi, ptotic kidney b) GI i) Appendicitis, IBD, sigmoid diverticular disease, rectosigmoi carcinoma 2) Evaluation of Ovarian disease a) Pre-puberty: ovaries should be non-palable b) Reproductive years: palpable (on OCP bilaterally equal); mass more likely to be benign c) Menopause: non-palpable if palpable warrants further investigation; mass more likely to be malignant d) Elevated CA 125 requires further investigation, but be careful because CA 125 has low specificity 3) Functional Ovarian Cyst a) Follicular cyst: failure of a mature follicle to rupture for ovulation (fluid: estrogen; lining is granulosa cells) i) Most of them spontaneously resolve on their own and are asymptomatic ii) Those that do not resolve on their own or become symptomatic (unilateral pain and alteration of menses) can be treated with OCP to encourage resolution. iii) Rupture of the cyst may cause acute pelvic pain -> surgery is not warranted b) Corpus Luteum Cyst i) Corpus luteum becomes cystic (1) Two types (a) Common corpus luteal cyst: (i) CP: missed menstrual period (prolonged due to cyst releasing progesterone), unilateral lower quadrant pain, and adnexal enlargement 1. Rule out ectopic pregnancy (ii) Resolve spontaneously, if recurrent may benefit from OCP (b) Luteal-phase cyst/corpus hemorrhagicum (i) Presents very similar to an ectopic pregnancy (ii) If bleeding is minimal may treat with analgesics and reassurance (iii) If bleeding is extensive requires surgical resection of bleeding cyst (iv) Usually present in those taking anticoagulant medication or have an inherited bleeding disorder c) Theca lutein cyst i) Observe in pregnancy and are bilateral; may become large and multicystic ii) Associated with pregnancy, moles, clomiphene citrate, hCG ObGyn Beckman 82

4) Benign Ovarian Neoplasms a) Epithelial Neoplasms: i) Serous cystadenoma: most common epithelial cell neoplasm; reproductive age: conservative treatment of removing on the disease part or unilateral oophrectomy; post-menopause: TAHBSO b/c of increase risk of malignant transformation ii) Mucinous cystadenoma: may become large and invade the pelvis iii) Endometroid: endometriomas -> cyst with well differentiated endometrial glands iv) Brenner cell tumor: solid tumor usually associated with mucinous cystadenoma; low rate of malignant transformation b) Germ Cell Neoplasm i) Benign cystic teratoma (dermoid cyst): (1) Most common ovarian neoplasm; may contain tissue from all three germ layers (with squamos tissue type being the most common): (2) Stroma ovarri: functioning thyroid tissue (3) CP: asymptomatic, unilateral, cystic adnexal mass that is mobile (4) Tx: surgical removal c) Stromal Cell Neoplasm i) Granulose theca cell tumor (1) High likelihood of malignancy (2) Produces estrogen -> pediatric precocious puberty/feminization ii) Sertoli-Leydig cell timor (1) Produces testosterone -> hirsutism and virillization iii) Ovarian Fibroma (1) Collagen production of spindle cells (2) Meigs syndrome: ovarian fibroma, ascites, and right pleural effusion d) More common than malignant, require surgical removal because of increase risk of malignancy transformation (risk of transformation increases with age); if truly benign may use conservative measures to preserve fertility 5) Malignant Ovarian Neoplasms a) CP: abdominal fullness/distension, abdominal/back pain, decrease in energy or lethargy, and increase in urinary frequency b) Most often is diagnosed in the advance stages b/c of lack of screening test (CA 125 is not a screening test, but and indicated with positive PE to determine malignancy) c) Risk factors: nullparity, endometriosis, primary infertility, BRCA1/2, and HNPCC d) Long term suppression of ovulation (OCP) have been found to decrease the incidence of ovarian cancer e) Histologic Classification i) May be associated with benign tissue and if so should remove both ovaries due to an increase risk of malignant tranformation f) Staging i) Confined to the ovaries ii) Local extension ObGyn Beckman 83

iii) Distant extension and node involvement iv) Mets g) Epithelial Cell Ovarian Carcinoma i) Most common type ii) Serous carcinoma: Bilateral, multiloculated cystic, and psammoma bodies iii) Mucinous cystadenocarcinoma: unilateral; mucious ascites called pseudomyxomatous peritonei iv) Risk factors: BRCA1, HNPCC (colon, ovarian, and endometrial, and breast cancer), positive first degree relative increase risk -> may desire to have BSO to decrease risk v) Clear cell carcinoma: derived from mesonephric ducts vi) Brenners carcinoma: benign and looks like bladder h) Endometroid: found with endometriosis and endometrial carcinoma i) Germ Cell Tumors: i) Dysgerminoma (1) Responds well to radiation and chemotherapy (2) Observed more often in young females (3) Generally unilateral and most common of the germ cell tumor (4) Less than 10 cm may be treated conservatively with surgery (5) Greater than 10 cm with nodal spread treat with cisplatin and bleomycin or etoposide (6) Spreads first through lymph nodes ii) Immature teratoma (1) Grows quickly and presents with abdominal fullness and pain (2) Observed more often in young females (3) If unilateral treat with unilateral oophrectomy and chemotherapy (responds well) iii) Rare germ cell tumor (1) Endodermal sinus tumor: produces AFP (2) Embryonal cell carcinoma: produces AFP and hCG j) Gonadal Stromal Cell Tumor; i) Granulosa cell tumor (1) Produces estrogen: increase risk of endometrial hyperplasia and carcinoma (2) Children: TAHBSO (3) + Children: conservative measures unilateral BSO ii) Sertoli-Leydig tumor: produced testosterone: hirsutism and virilization k) Other Ovarian Cancers: i) Initial manifestation of primary lymphoma ii) Malignant mesodermal sarcoma: aggressive and poor prognosis 6) Cancer Metastatic to the Ovary a) Kruckenburg tumor i) Ovarian tumor from other sites most commonly GI or breast ii) Inifiltrative mucinous carcinoma of a signet ring cell type bilaterally b) History of GI or breast cancer want to consider BSO at the time of TAH 7) Fallopian Tube Disease ObGyn Beckman 84

a) Benign disease: paraovarian cysts (mesosalpinx and are vestigal wolfian ducts structures) paratubal cysts/hydatid cysts of morgani (fimbrated end of the fallopian tube) b) Carcinoma of the Fallopian Tube: i) CP: post-menopausal bleeding and abnormal vaginal bleeding; hydrotubae profluens diagnostic of the tumor ii) However, it is more common to have cancer extension from the ovaries or uterus 8) Management of ovarian and fallopian tube carcinoma a) Cytoreductive surgery: pelvic washings, inspection and palpation of the abdominal organs including the omentum, partial omentectomy, sampling of pelvic and periaortic nodes b) Chemotherapy: carboplatin and paclitaxel ObGyn Chapter 47: Human Sexuality 1) Human Sexual Response a) Traditional based model i) Desire Arousal Plateau Orgasm Resolution b) Intimacy based model i) Intercourse is a means to be closer to your partner ii) Integrates psychological and physical aspects of sex iii) Page 416, Figure 47.2 2) Factors Affecting Sexuality a) Depression b) Medication (anti-depressant medications that do not decrease sexual drive: nefazodone, mirtazipine, bupropion, venlaxafine, and buspirone) c) Low estrogen/testosterone d) Psychologic factors 3) Screening Questions a) Are you sexually active, satisfied; do you think your partner is satisfied; do you have any questions or concerns about sexual functioning? Evaluate sexually abuse history. 4) Drugs Affecting Sexual Response a) Page 420, Box 47.2 5) Establishing a Diagnosis a) Page 422, Figure 47.4

ObGyn Beckman 85