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OBGYN End of Rotation Exam – Outline
Female Reproductive Physiology
 Hypothalamic-pituitary-ovarian axis
o Neurohypophysis (Oxytocin, ADH)
 Consists of the posterior lobe, neural stalk, median eminence
 Derived from neural tissue
 In direct continuity w/the hypothalamus and CNS
o Adenohypophysis (FSH, LH, TSH, prolactin, GH, ACTH)
 Consists of the pars distalis, pars intermedia & pars tuberalis
 Surrounds the neural stalk and is derived from ectoderm
 Arterial blood supply to median eminence = major avenue of transport for hypothalamic secretions
to the ANTERIOR pituitary
 FSH, LH, TSH and b-hCG have the same alpha unit
 Pituitary release of prolactin is under tonic inhibition by the hypothalamus
 Menstrual cycle
o Follicular phase begins with the onset of menses and ends w/the pre-ovulatory surge of LH
o Luteal phase begins with the onset of the pre-ovulatory LH surge and ends with the 1st day of menses
 BOTH LH and FSH are suppressed via (-) feedback of elevated estradiol and progesterone
o Decreasing levels of estradiol & progesterone from the regressing CL of the preceding cycle initiate an incr.
in FSH  stimulation of follicular growth and estradiol secretion
o LH stimulates the theca cells to produce androgens
o FSH stimulates the granulosa cells to convert androgens into estrogens
o At LOW levels of estradiol there is (-) feedback on LH
o As estradiol levels rise, (+) feedback  LH surge and ovulation
o Menstruation generally occurs 14 days AFTER the LH surge
 Phases of the Endometrium
o Proliferative phase
 Characterized by endometrial proliferation to ESTROGENIC STIMULATION
 Incr. estrogen  cellular proliferation of the epithelial lining, endometrial glands and ct of the
stroma
 Incr. in the length of the spiral arteries (traverse almost the entire thickness of the endometrium)
 Spiral Aa. elongated and convoluted
 Endometrial glands are straight w/narrow lumens
o Secretory Phase
 Following ovulation, progesterone secretion by the CL stimulates the glandular cells  tortuous
and dilated/filled lumens
 Spiral Aa. extend into the superficial layer of the endometrium and become convulated
 If pregnancy does not occur by day 23, the CL begins to regress, secretion of progesterone and
estradiol declines and the endometrium undergoes involution
 Constriction of the spiral arterioles occurs 1 day before onset of menstruation, followed by leuko.
infiltration of RBC extravasation
 Occur secondary to PG production by endometrium
Obstetrics and Osteopathy
 Causes of pelvic pain in the female patient
o Endometriosis, adenomyosis, Mittelschmerz, infection
 MSK treatment for Carpal Tunnel Syndrome in pregnant patients
o Direct Stretching of the transverse carpal ligament, active articulation of the carpal bones and treatment of
pectoral girdle/upper thoracic (sympathetic supply to the UE) somatic dysfunction  decr. Median N.
compression
 Sacral Inhibition
o To DECREASE the severity of dysmenorrheal
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Physician stand to one side at the level of the patient’s pelvis w/one hand palm down along the vertical axis
of the sacrum and other hand plam down over the first hand
o Apply pressure slowly to the sacrum through the arms
o Apply as much weight as is tolerable to the patient and hold steadily for 1-2 mins.
o Release the pressure very slowly
Differentiate between viscerosomatic/somatovisceral/somatosomatic/and viscerovisceral reflexes
o Somatovisceral /Viscerosomatic is hyperactivity in visceral afferent nerves due to visceral disease or
dysfunction  segmentally related reflex somatic dysfunction
Sympathetic & Parasympathetic viscerosomatic reflexes of the female pelvic organs
o Ovaries T10-T11, Uterus T9-L2, Fallopian tubes T10-L2
o Parasympathetic innervation of the female GU tract via pelvic splanchnic nerves S2-S4
o Lateral half of the fallopian tubes receives parasympathetic innervation from the Vagus nerve
Anterior/Posterior sacral dysfunctions
o A posterior sacrum is often accompanied by spasm in the piriformis muscle
o An anterior sacrum can cause spasm of the gluteus medius
Causes of primary and secondary somatic dysfunction of the pubic symphysis and pelvis
o Dysfunction of the symphysis pubis is seen both ante and post-partum and following strenuous use of the
ADDuctor muscles
o Primary psoas somatic dysfunction is in the UPPER half of the lumbar spine producing psoas spasm
 Type II mechanics of L1 on L2 or L2 on L3, typically in flexion w/rotation and side-bending TOWARD
the side of the tight psoas
o Secondary psoas somatic dysfunction is in the presence of lumbosacral inflammation or instability
 Physiologic splinting of the surrounding musculature  psoas spasm.
 Forward displacement of the patient’s center of gravity as the gravid uterus grows  incr. stress
upon the LS junction and psoas spasm
Osteopathic approach to the obstetric patient
o Structural evaluation
 Start with the patient standing and monitor the gait
 Evaluate spinal AP curves
 The transition b/w the thoracic kyphosis and lumbar lordosis shifts upward b/w T11-T8
o Look at all bilateral landmarks from the mastoid processes down to the greater trochanters
o Evaluate a standing flexion test and look for paravertebral prominences associated with type I dysfunction
o When the patient is seated, assess for SI restriction and motion, palpate the sacral sulci and assess torso
rotation
o Assess for TART at the superior and inferior poles of the SI joints and at the T/L junction
o With the patient supine, evaluate the rest of the MSK system noting any abnormalities in the OA, T/L, L/S
transition areas
o Palpate the sacrum to assess for restriction of articular motion and to assess the inherent sacral motion of
the CRI
o Check anterior counterstrain points, innominate and pubic bone dysfunction
o Correction of inequality of leg length (responsible for CHRONIC sacral somatic dysfunction), may be a prime
factor in the treatment of patho-physiologic changes affecting the pelvic organs
o Dysmenorrhea is CRAMPING pelvic pain that can be treated by targeting the T/L somatic dysfunction to
reduce sympathetic input to the uterus  relaxation
**Look at page 123 and know how to do myofascial release of the ischial tuberosity!!!***
Maternal-Fetal Physiology
 Discuss the maternal physiologic anatomic changes associated with pregnancy
o Retention of Na/H20 during pregnancy  total blood volume incr. of about 40%
o Disproportionate incr. in plasma voL. compared to the RBC voL.  hemodilution & a decr. Hct (anemia of
pregnancy)
 Physio. functions of the placenta and fetus
o Perfusion of the intervillous spaces of the placenta with maternal blood allows the transfer of nutrients and
oxygen from the mother to the fetus
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Nutrient transfer to the fetus occurs via both active and passive transport
o
IgG antibodies can pass through the human placenta  protection to the fetus in utero
o
Placenta secretes hormones (via syncytial layer/syncytiotrophoblast of chorionic villi) that are important
during pregnancy.
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hCG = 1st placental hormone produced
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Found in maternal blood and urine as early as the first missed menstrual period (shortly
after implantation has occurred
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Blood serum will be completely negative for hCG 1-2wks after birth
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hCG testing = proof that all placental tissue is delivered
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Present only during pregnancy because it is secreted by the placenta
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Ensures the CL continues to secrete progesterone and estrogen
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Suppresses the maternal immunologic response so that placenta is not rejected
hPL (Human Chorionic Somatomammotropin)
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Promotes mammary gland growth in preparation for lactation
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Regulates maternal glucose, protein, and fat levels so that this is always available to the
fetus
Estrogen
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Stimulates the development of secondary female sex characteristics
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Contributes to mammary gland development in preparation for lactation
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Stimulates uterine growth to accommodate growing fetus
Progesterone
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Maintains endometrial lining of the uterus during pregnancy
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Prevents preterm labor by reducing myometrial contraction
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Discuss the effect of pregnancy on common diagnostic studies – see charts on pages 57, 59, 62 & 63
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Describe how certain medical conditions affect pregnancy
o Smoking and alcohol are associated with increased incidence of chromosomally normal abortions
o DM, hypothyroidism and SLE are linked to spontaneous abortion
History of genetic abnormalities
o Couples should receive preconception counseling before they decide to have children
o Women >34yo have an increased risk for having children w/chromosomal abnormalities
o Indications for genetic counseling:
 Previous child with or a family history of birth defects, chromosomal abnormality or known genetic
disorder
 Previous child w/undiagnosed MR
 Previous baby who died in the neonatal period
 Multiple fetal losses
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 Abnormal serum marker screening results
 Consanguinity
 Maternal conditions predisposing the fetus to congenital abnormalities
 Current pregnancy history of teratogenic exposure
 Fetus with suspected abnormal US findings
 Parent who is a known carrier of a genetic disorder
Advanced maternal age
o Chances of abortion increase with increased maternal age
o Risk is >10% if ≥40yo and >50% at 45yo (due to incr. incidence of chromosomal abnormalities)
Nutrition and exercise
o Women should not fast b/c  ketosis and preterm delivery
o Women should have 5 feedings/day and NEVER skip breakfast
o Normal pregnancy requires an incr. in daily caloric intake of 300 kcal
o Fatigue usually abates by the 4th month of pregnancy
o Work that requires prolonged standing, shift or night work and high cumulative occupational fatigue has
been associated w/an increased risk for low birth weight and prematurity
o Women should be advised to continue to exercise during pregnancy, unless there is pregnancy-induced
HTN, preterm labor or rupture of membranes, intrauterine growth restriction, incompetent cervix,
persistent 2nd or 3rd trimester bleeding
Medications and environmental hazards
o Teratogen = any agent/factor that can cause abnormalities of form or function in an exposed fetus
o Thalidomide phocomelia
o Efficacy is dependent on the genetic makeup of both mother and fetus
o Two principles of teratogens are dose (how much was given) and timing (referring to what is developing in
the fetus when the teratogen exposure occurs)
o Examples: EtOH, anti-anxiety drugs (meprobamate, chlordiazepoxide, fluoxetine), antineoplastic agents
(aminopterin, methotrexate), alkylating agents (busulfan, chlorambucil, cyclophosphamide, nitrogen
mustard), anticoagulants (coumarin derivatives, heparin)
Immunizations
o Rh- women should receive RHo-GAM at 28wks AND postpartum
o Rubella vaccination is contraindicated during pregnancy
 Pregnant women who are seronegative should be vaccinated IMMEDIATELY postpartum
o Syphilis testing is MANDATED by law
o Women who test neg for HBsAg and are at high risk for HepB are candidates for vaccination before and
during pregnancy
 Infants born to HBsAg+ mothers should receive both HBIG and HepB vaccine w/in 12hrs of birth
followed by 2 more injections of HepB vaccine in the first 6mos of life
Intrapartum Care
 True and false labor
o True labor = progressive cervical effacement AND dilation resulting from regular uterine contractions that
occur at least every 5mins and last 30-60secs
o False labor (Braxton hicks contractions) = contractions that are NOT associated with progressive cervical
dilation or effacement
 Initial assessment of the laboring patient
o Cervix is noted to soften as a result of increased water content and collagen lysis
o Effacement occurs as it is taken up into the lower uterine segment  release of the mucous plug
o Onset of labor may be heralded by the passage of a small amount of blood-tinged mucus (“bloody show”)
 Stages/mechanism of normal labor and delivery
o 1st stage = latent (cervical effacement and early dilation) and active (rapid cervical dilation)
 Entire length is retracted into the lower uterine segment
 The lateral recumbent position should be encouraged to ensure perfusion of the uteroplacental
unit
 AFTER completion of cervical dilation the second stage begins
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At the beginning of the 2nd stage, the mother usually has a desire to bear down with each contraction
 Fetal descent must be monitored by measuring progress of the presenting part through the birth
canal
 Usually takes from 30mins – 3hrs in primigravid women and 5-30mins in multigravid
women
 Six movements of the baby enable it to adapt to the maternal pelvis
 Descent, flexion, internal rotation, extension, external rotation and expulsion
 Descent is brought about by the force of the uterine contractions, maternal bearing down efforts
and gravity
 Flexion exists before labor as a result of the natural muscle tone of the fetus
 In the occipitoanterior position, the effect of flexion is to change the presenting diameter
from the occipitofrontal to the small suboccipitobregmatic.
 In the occipitoposterior position, complete flexion may not occur  larger presenting
diameter = longer labor.
 Internal rotation = head rotates so the occiput turns anteriorly toward the symphysis pubis
 Does not occur until the child has met a zero station
 Extension must occur before the head can pass through the pelvis
 Vertex has reached a station of +5 and when necessary an episiotomy may aid in reducing
perineal resistance
 External rotation is to help the shoulders align themselves anteroposteriorly within the pelvis
o 3rd Stage involves the delivery of the placenta AFTER the cervix and vagina are thoroughly inspected
 Signs of placental separation:
 Fresh show of blood from the vagina
 Umbilical cord lengthens outside the vagina
 Fundus of the uterus rises up
 Uterus becomes firm and globular
o 4th Stage of labor is the hour IMMEDIATELY following delivery
 BP, HR, and uterine blood loss must be monitored closely
 Postpartum hemorrhage occurs during this time b/c of uterine relaxation, retained placental
fragments or unrepaired lacerations
Evaluation of labor progress
o Check cervical effacement and dilation as well as fetal station
o Assess fetal heart rate
o Monitor uterine contractions every 30mins via palpation
Pain management during labor
o Nonpharmacologic methods:
 Education and psychoprophylaxis, emotional support, back massage, hydrotherapy, biofeedback,
transcutaneous electrical nerve stimulation, acupuncture and hypnosis
 Work best early in the first stage of labor when the pain is least intense
o Pharmacologic treatment
 Parenteral narcotics, regional analgesia and inhalational analgesia
 Parenteral narcotics work best in the EARLY 1st stage when the pain is primarily visceral
 All opioids readily cross the placental barrier and may cause neonatal respiratory depression
 Fentanyl and nalbuphine have the shortest neonatal half lives
 Neuraxial analgesia = most effective form of pain relief
 Lumbar epidural analgesia = most common form
 Epidural is to achieve a T10 sensory level block followed by an infusion of a dilute solution of the
same agent until delivery (pain during the first stage of delivery is b/w T10-L2)
 A PUDENDAL NERVE BLOCK ANESTHETIZES SOMATIC AFFERENT NERVE FIBERS ENTERING THE
SPINAL CORD AT S2-S4.
 Effective at relieving the perineal pain of the 2nd stage of labor
 For elective urgent cesarean delivery, regional anesthesia is preferred b/c the airway is maintained
 If no epidural is in place, a spinal block is frequently used
 General anesthesia is employed for C-sections in 3 situations:
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 Extreme urgency w/o a pre-existing, functional epidural catheter
 There is a contraindication to regional anesthesia
 Regional anesthesia has failed
Methods of monitoring the mother and fetus
o Mother
 Blood screen for rhesus, HepB, check voided urine for presence of protein and glucose
 Uterine contractions monitored every 30mins by palpation for their frequency, duration and
intensity
 For high risk pregnancies, uterine contractions should be monitored continuously + fetal HR
 Vaginal exams should be done sparingly to decrease the risk for intrauterine infection
o Fetal
 HR should be evaluated by auscultation with a De Lee stethoscope, by external monitoring with
Doppler equipment or by internal monitoring with a fetal scalp electrode
Management of normal delivery
o When delivery is imminent, the patient is usually placed in the lithotomy position and the skin over the
lower abdomen, vulva, anus and upper thighs is cleansed with an antiseptic solution
o Uncomplicated deliveries may be carried out in the supine position with the thighs flexed
o As the perineum becomes flattened by the crowning head, an episiotomy may be performed to prevent
perineal lacerations
o To facilitate delivery of the head, a Ritgen maneuver may be performed
 The right hand exerts upward pressure through the distended perineal body, first to the
supraorbital ridges and then to the chin
 This upward pressure increases extension of the head and prevents it from slipping back b/w
contractions
o Once the head is delivered, the airway is cleared of blood and amniotic fluid
 Suction of the nares is not performed if fetal distress or meconium stained liquid is present 
gasping and aspiration of pharyngeal contents
o After the airway has been cleared, an index finger is used to check whether the umbilical cord is wrapped
around the neck
o Following delivery of the head, the shoulders descend and rotate into the anteroposterior diameter of the
pelvis and are delivered
o After delivery, blood will be infused from the placenta into the newborn if the baby is held below the
mother’s introitus
 Cord is clamped and cut within 15-20 seconds
 Delayed clamping  neonatal hyperbilirubinemia as additional blood is transferred from the
placenta to the newborn
Vaginal repair
o Midline episiotomy
 A taped sponge is placed in the upper vagina and a continuous locked 00 or 000 absorbable suture
closes the vaginal epithelium from the apex to the hymeneal ring
 Three interrupted sutures are used to close the deep perineal fascia (of Colles) and underlying
levator ani muscles
 The vaginal epithelial suture is brought below the skin into the sub-q tissue and the same
continuous suture is used to close the superficial fascia down to the anal edge of the episiotomy
 The same suture is used as a subcuticular stitch coming back to the hymeneal ring, where it is
doubly tied
 Repair of a 3rd degree tear involves approximating the fascia surrounding the rectal sphincter
muscle and re-approximating the vaginal tears with locked continuous sutures
Indications for operative delivery (pgs. 222-223)
o Prolonged second stage labor
o Suspicion of immediate or impending fetal compromise
o To stabilize the aftercoming head during a breech delivery
o To shorten the second stage of labor for maternal benefit
Immediate postpartum care
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The mother must be monitored very closely the first hour after delivery to evaluate BP, HR and uterine
blood loss
Occult bleeding may manifest as pelvic pain or an increase in pulse rate out of proportion to any decrease
in BP
 May indicate hypovolemia
Postpartum Care
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Postpartum Hemorrhage
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Defined as blood loss in excess of 500mL at the time of vaginal delivery
Most of the blood loss occurs from the myometrial spiral arterioles and decidual veins that previously
supplied and drained the intervillous spaces of the placenta
o Causes of PP hemorrhage:
 Uterine atony (75-80%), genital tract trauma, retained placental tissue, low placental implantation
 Uterine inversion, coagulation disorders, abruptio placentae
 Amniotic fluid embolism, retained dead fetus and inherited coagulopathy
o dDx of postpartum hemorrhage
 Fundus of the uterus should be palpated through the abdominal wall to determine the presence or
absence of uterine atony
 Thorough inspection of the vagina and cervix should be performed to ascertain whether any
lacerations may be compounding the bleeding problem
 Any uterine inversion or pelvic hematoma should be excluded during the pelvic exam
 If no cause for the bleeding is found, a coagulopathy must be considered
o Immediate management
 Identification of patients at risk and the institution of prophylactic measures during labor to
minimize the possibility of maternal mortality
o Inspection for lacerations
 Cervical lacerations need not be sutured unless they are ACTIVELY bleeding
 For vaginal repair good tissue exposure is important and a running lock suture technique provides
the best hemostasis
 Large expanding hematomas of the genital tract require surgical evacuation of clots
 Stable hematomas can be observed and treated conservatively
o Use of uterine contractile agents
 Analogues of PG F2alpha given IM are effective in controlling postpartum hemorrhage caused by
uterine atony
 The 15-methyl analogue has a more potent uterotonic effect and longer duration of action
 Failing pharmacologic treatment, a bimanual compression and massage of the uterine corpus may
control the bleeding and cause the uterus to contract
 Operative intervention is last resort.
o Management of volume loss
 Make sure an adequate supply of type specific blood is available and run it through a large bore
needle or catheter before delivery
 Also have LR to infuse to restore intravascular volume
o Management of coagulopathy
 The specific defect should 1st be corrected by the infusion of blood products
 Patients with thrombocytopenia require platelet concentrate infusions and those with vWD require
factor VIII concentrate or cryoprecipitate
 A packed RBC infusion is given to a patient who has bled enough to drop the circulating red cell
population sufficiently to comprise the delivery of O2 to the tissues
 A blood transfusion is best judged by symptoms of O2 deprivation
 Thrombocytopenia is the most common abnormality
 FFP may be transfused for prolonged PT or hypofibrinogenemia.
Postpartum Infection
o Risk factors
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Poor nutrition and anemia
PROM, prolonged rupture of the membranes, prolonged labor
Frequent vaginal examinations during labor, C-section, forceps or vacuum delivery
Cervical or vaginal lacerations, manual removal of the placenta, retained placental fragments or
fetal membranes
dDx of infectious organisms
 Vaginal flora during gestation resembles the non-pregnant state although there is a trend toward
isolating mycoplasma genitalis and anaerobic strep in the last trimester
 Potentially pathogenic organisms cultured from the vagina include enterococci, hemolytic and nonhemolytic strep, anaerobic strept, enteric bacilli, pseudo-diphtheria and neisseria species
 Aerobic organisms include E.coli and mixed infections with bacteroides fragilis
Evaluation and patient management
 Evaluation of a FEBRILE postpartum patient should include a careful history and PE
 Extra-pelvic causes of fever such as breast engorgement, mastitis, aspiration pneumonia,
atelectasis, pyelonephritis, thrombophlebitis or wound infection should be excluded
 Pelvic exam may allow the palpation of tender, thrombosed and edematous ovarian, parauterine or
iliac veins
 Diagnosis is usually made by exclusion and by the prompt regression of fever following
commencement of heparin
 Before you start Abx for puerperal endometritis, aerobic and anaerobic cultures should be obtained
from the blood, endocervix and uterine cavity, and a catheterized urine specimen obtained for
culture
Indications for the use of prophylactic antibiotics
 Early Abx should be instituted to confine and then eliminate the infectious process
 The Abx should provide anaerobic coverage b/c these organisms are involved in 70% of puerperal
infections
 Abx should be continued for at least 48hrs after the patient becomes afebrile
 Anaerobic organisms require prolonged therapy for elimination
 Broad spectrum Abx such as ampicillin and cephalosporins are effective 1st line drugs for mild and
moderate cases of puerperal infection
 Major pelvic pathogen RESISTANT to 1st line combo (penicillin/aminoglycoside) is BACTEROIDES
FRAGILIS
 Treat w/clindamycin
Complications of Pregnancy
 Ectopic Pregnancy
o dDX for first trimester bleeding
 Abortion, cervicitis, cervical polyps, subchorionic hemorrhage, decidual tissue, implantation
bleeding, period during pregnancy, ectopic pregnancy
o Risk factors predisposing patients to ectopic pregnancy
 History of tubal infection, smoking, prior ectopic, history of tubal sterilization w/i the past 1-2yrs
 History of tubal reconstructive surgery, pregnancy with current IUD, Depo or emergency
contraceptive pill use, infertility due to tubal factors, use of assisted reproductive technology
o Symptoms and physical findings suggestive of ectopic pregnancy
 CLASSIC TRIAD = prior missed menses, vaginal bleeding and lower abdominal pain
 Acutely ruptured
 Patient presents with severe abdominal pain and dizziness
 May also c/o ipsilateral shoulder pain from phrenic nerve irritation caused by the blood in
the upper abdomen
 Signs of hemodynamic instability (tachycardia, diaphoresis, hypotension, LOC)
 Abdomen may be distended and acutely tender with guarding and rebound tenderness
 Patient usually has cervical motion tenderness and a slightly enlarged, globular uterus
 Probably ectopic
 Patient presents with lower pelvic pain and vaginal spotting with or without amenorrhea
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 There may be a variable amount of fluid in the cul-de-sac
 Double-ring sign in the adnexa on occasion
 A corpus luteum cyst is often present
o Methods and tests to confirm ectopic pregnancy
 Diagnosis can be confirmed by the ABSENCE of IUP on US in a woman with a high hCG
 Quantitative hCG, TVUS and office curettage
 An abnormally rising hCG level of >2000 with no gestational sac seen on US is DIAGNOSTIC
 Serum progesterone levels >25 ng/mL can reliably indicate a normal IUP and levels less than
5ng/mL are consistent with an ABNORMAL pregnancy
o Treatment options
 Laparotomy is the PREFERRED surgical approach for women who are hemodynamically unstable b/c
rapid access to the bleeding site is critical
 Salpingectomy is recommended when there has been significant damage to the tube
 Salpingotomy is when the incision is closed instead of open
 Methotrexate therapy is another consideration, especially when the ectopic is unruptured
 Surgical intervention is required if the patient becomes symptomatic
Spontaneous Abortion
o Types of spontaneous abortion
 Threatened: when a pregnancy is complicated by vaginal bleeding BEFORE the 20th week
 Inevitable: complicated by BOTH vaginal bleeding and cramp-like lower abdominal pain
 Incomplete: vaginal bleeding, cramp-like pain and cervical dilation that involves the passage of
products of conception
 Complete: passage of ALL the products of conception
 Missed: the fetus has died but is retained in the uterus, usually >6wks
 Recurrent: three successive spontaneous abortions
o Complications of spontaneous abortion
 Infection may occur if any tissue from the placenta or fetus remains in the uterus after the
miscarriage
 Symptoms of an infection: fever, vaginal bleeding that does not stop, cramping and a foul-smelling
vaginal discharge
Septic abortion
o Can occur when bacteria enters the uterus
o The bacteria may also belong to the vaginal flora
o STI’s such as chlamydia may also cause septic abortion
Medical and Surgical Conditions in Pregnancy
 Gestational Diabetes
o Incidence and risk factors
 Rate of 3-8% of GDM
 Pregnancy is associated with progressive insulin resistance
 hPL, progesterone, prolactin, cortisol and TNF are associated with incr. insulin resistance during
pregnancy.
o Defined as glucose intolerance with onset or first recognition during pregnancy
o Pre-gestational diabetes is when a woman has diabetes before they get pregnant and it is continued during
pregnancy
o White’s classification is helpful in assessing disease severity and the likelihood for complications
 Also distinguishes b/w gestational diabetes and pre-gestational diabetes
o Screening and diagnosis
 Screening is usually performed b/w 24-28wks with a 50g 1hr oral glucose challenge test
 If the level exceeds 200mg/dL, a F/U glucose tolerance test is NOT needed for diagnosis
 Screening is advised at the first prenatal visit in pregnant women with risk factors such as maternal
age >25yrs, previous macrosomic infant, previous unexplained fetal demise, previous pregnancy
with GDM, family history of diabetes, history of PCOD and obesity
 If the first trimester screen is negative it should be repeated at 24-28wks
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Glucose values above 130-140 are considered abnormal and have 80-90% sensitivity in detecting
GDM
 An abnormal screening is followed with a diagnostic 3hr 100g oral glucose tolerance test
 This involves checking the fasting blood glucose after an overnight fast, drinking a 100g
glucose drink and checking glucose levels hourly for 3hrs
o See chart on pg. 193 for maternal and fetal complications of gestational and pre-gestational diabetes
o Management and monitoring of gestational and pre-gestational diabetes
 Caloric requirements are calculated on the basis of ideal body weight
 Diet comprised of 50% CHO, 20% protein, 20% fat
 Should also contain generous amount of fiber
 Oral hypoglycemic agents have NOT been recommended for pregnant women b/c of the risk for
teratogenesis
 CAN be used AFTER the first trimester
 Insulin = GOLD STANDARD
 Diabetic patients should be encouraged to engage in mild to moderate aerobic exercise for about a
½ hour after meals
Pre-eclampsia/Eclampsia Syndrome
o Definitions and classification of HTN in pregnancy
 The diagnosis of HTN should be reserved for patients with a systolic BP ≥140mmHg or a diastolic BP
≥90mmHg.
o Pathophysiology
 Pre-E is a syndrome unique to pregnancy characterized by the NEW ONSET of HTN and proteinuria
in the latter half of gestation
 No single, definitive cause has been identified.
 One of the primary underlying pathophysiologic abnormalities is vasospasm
 Eclampsia is the presence of tonic-clonic seizures in a woman with pre-E that cannot be attributed
to other causes
o Symptoms, physical findings and diagnostic methods
 Two criteria essential for diagnosis of preeclampsia:
 The development of HTN in a woman whose BPs were previously normal after the 20th
week of pregnancy
 The development of NEW ONSET proteinuria after the 20th week of gestation (≥0.3g protein
in a timed, 24hr urine collection)
 Severe preeclampsia
 Systolic BP ≥160mmHg or diastolic BP ≥110mmHg at rest at least 6hrs apart
 Heavy proteinuria (at least 5g in a 24hr collection or a value of 3+ in urine samples collected
3hrs apart)
 Oliguria (<500mL in 24hrs)
 Cerebral or visual disturbance, pulmonary edema or cyanosis, epigastric or RUQ pain,
impaired liver function, thrombocytopenia, fetal growth restriction
 Renal BF and GFR are significantly LOWER
 Afferent vasoconstriction  damage to the glomerular membranes  incr. permeability to
proteins  proteinuria
 High cerebral vascular resistance
 Activation of the coagulation system
 Weight gain and edema
 Increase in serum uric acid concentration
 In the liver, vasospasm may result in focal hemorrhages and infarctions  RUQ or epigastric pain
and elevated serum enzyme levels
o Approach to management
 Delivery is the ONLY definitive cure for pre-E
 A woman with mild pre-E or whose disease does not appear to be progressing will not be delivered
unless gestation is ≥37wks or older

o
Women with severe pre-E should usually be delivered after a period of stabilization, regardless of
gestational age of the fetus
 Fetal examination and NST
 If the mother’s disease is mild and there is no evidence of fetal compromise, rest and observe
 Medical control of severe HTN and corticosteroids for fetal lung maturity will moderate the disease
process and allow delivery to be delayed
 Seizure prophylaxis with magnesium sulfate should be instituted during the intrapartum period and
continued for 24hrs after delivery
 Safest/most efficacious drugs for the acute control of severe HTN = labatelol and hydralazine
 Oral nifedipine should be used cautiously to avoid hypotension
 Pharmacologic stabilization of eclampsia = preventing recurrent convulsions and controlling HTN
 Magnesium sulfate is the most efficacious drug for preventing recurrent eclamptic
seizures and has the best safety profile for mother and fetus
Maternal and fetal complications
 Pregnancies complicated by severe preterm pre-E are at a higher risk for CV disease later in life and
at very high risk for recurrent pre-E in subsequent pregnancies
 Women with gestational HTN have a higher incidence of developing chronic HTN later in life
 Female offspring of pre-E women experience an increased risk for pre-E in their own pregnancies
Isoimmunization
 Role of red blood cell Ags
o The Rh complex is made up of a number of antigens incl. C, D, E, c, e and other variants such as D(U)
antigen
o >90% of Rh isommunizations are due to antibodies to D antigens
 Clinical circumstances under which D isoimmunization is likely to occur
o The occurrence of an undetected placental leak of fetal RBCs into the maternal circulation during pregnancy
o “Grandmother” theory
 Suggests that an Rh- woman may have been sensitized from birth by receiving enough Rh+ cells
from her mother during her own delivery to produce an Ab
o 1st exposure  primary sensitization, whereas the 2nd causes an anamnestic response  rapid production
of Igs  a “transfusion reaction” or hemolytic disease of the fetus
o The initial response to exposure to Rh antigen is the production of IgM Abs, followed by the production
of IgG Abs that are CAPABLE OF CROSSING THE PLACENTA
 If the fetus has the Rh antigen, these Abs will coat the fetal RBCs and cause hemolysis
o Most immunizations occur at the time of delivery and Abs appear either during the postpartum period or
following exposure to the antigen in the next pregnancy
 Ig prophylaxis during pregnancy
o Indications for the use of Rh Ig
 Any antepartum event (such as amniocentesis) that may increase the risk for transplacental
hemorrhage
o Routine prophylactic administration of Rh Ig at 28wks is now the STANDARD OF CARE
 Determination of maternal isoimmunization and the severity of fetal involvement
o In Rh- patients whose anti-D Ab titers are positive, the blood group and Rh status of the father of the baby
should be determined
 If the father is Rh-, the fetus will be Rh negative
 If the father is Rh+, his Rh genotype and ABO status should be determined
o In an initially immunized pregnancy, the fetus is not in serious jeopardy if the titer remains BELOW 1:16
o Amniocentesis is the most commonly employed method to test fetal blood type
o The Liley chart can be used to determine the severity of the disease and the appropriate management at
27wks
o Percutaneous umbilical cord sampling can allow measurement of fetal H/H, blood gases, pH and bilirubin
Multi-fetal Gestation and Mal-presentation
 Etiology of monozygotic, dizygotic and multi-zygotic gestation
o



Monozygotic twins (splitting of embryo)
 Arise from cleavage of a SINGLE FERTILIZED EGG at various stages during embryogenesis
 The arrangement of the fetal membranes and placentas will depend on the time at which the
embryo divides
 Includes dichorionic/diamniotic, monochorionic/diamniotic and monochorionic/monoamniotic
o Dizygotic twins (fertilization of two or more eggs produced in single menstrual cycle)
 Arise from SEPARATE eggs
 Structurally distinct pregnancies co-existing in a SINGLE UTERUS, each with its own amnion,
chorion, and placenta
Altered physiologic state
o Maternal blood volume may increase by ≥3L
o Increased blood volume and demand for iron and folate increases the risk for anemia in the mother
o Pre-E and gestational HTN are almost doubled in multi-fetal gestation
o Maternal respiratory embarrassment, orthostatic hypotension due to compression of the vena cava and
aorta and compromise of renal function due to compression of the ureters
Symptoms, physical findings and diagnostic methods
o Historical factors such as a maternal family history of dizyogotic twinning, the use of fertility drugs, a
maternal sensation of feeling larger than with previous pregnancies or a sensation of excessive fetal
movements
o XS weight gain, XS uterine fundal growth and auscultation of fetal heart rates in separate quadrants of the
uterus
o Diagnosis requires a sonographic exam demonstrating two separate fetuses and heart activities and can
be made as early as 6wks
Approach to management
o Antepartum
 Management schemes are directed at prolonging gestation and increasing birth weight in order to
decrease perinatal morbidity and mortality
 Between 16 and 22wks, the patient is seen every 2wks for ultrasonographic cervical length
assessment
 During the third trimester, prevention of prematurity = KEY!
 The patient is monitored closely for pre-E,
 NST or BPP weekly from 36wks on
o Intrapartum
 A secondary or tertiary care center, a delivery room equipped for immediate C/S, a well-functioning
large-bore IV line, blood for transfusion, continuous monitor of FHRs, imaging techniques for
presentation of twins
o Postpartum
 Twins experience a 4x increase in cerebral palsy, low birth weight, prematurity and IUGR may
predispose to permanent brain injury
 Twins are shorter and lighter than singletons of similar birth weight until 4yo
Fetal Death
 Causes
o 1st trimester
 Chromosomal abnormalities
o 2nd trimester
 Uterine abnormalities
o 3rd trimester
 Cannot be determined in about 50% of cases but assoc. causes include HTN, DM, erythroblastosis
fetalis, umbilical cord accidents and fetal congenital anomalies
 Symptoms, physical findings and diagnostic methods for confirmation
o When the patient reports the absence of fetal movements, particularly if the uterus is small for date or fetal
heart tones are not detected, suspect fetal death
o A positive PG test does NOT work b/c the placenta continues to produce hCG
o


Diagnostic CONFIRMATION = real-time ultrasonography
 Detects the lack of fetal movement and absence of fetal cardiac activity
Patient management
o Watchful expectancy and induction of labor
o Management of women who fail to go into labor spontaneously = active intervention by IOL or D&E
o Justifications for IOL = emotional burden on the patient assoc. with carrying a dead fetus and slight
possibility of chorioamnionitis
o 10% risk of DIC risk when the baby remains in the uterus for >5wks
o Use of PGE2 or Dinoprostone b/w 12-28wks
o After 28wks, if condition of cervix favorable, misprostol followed by oxytocin is TREATMENT OF CHOICE
Maternal complications
o Monitor coagulopathy for DIC with weekly fibrinogen levels + Hct and platelet counts
 If fibrinogen level is decreasing, suspect DIC
o Elevated PT and PTT and decreased platelet count clarify the diagnosis
o Feto-maternal hemorrhage, TORCH infections, Listeria
o Guilty and angry patients should be referred to a bereavement support group
Abnormal Labor
 Abnormal labor patterns
o Abnormalities of the latent phase
 Labor exceeds 20hrs for nulliparous patients and 14hrs for multiparous patients
 May be caused by dysfunctional labor, premature or excessive use of sedatives or analgesics, fetal
mal-position or fetal size
 Patients have false labor with no progressive dilation of the cervix
o Abnormalities of the active phase
 Cervical dilation of <1.2cm/hr in nulliparous patients and <1.5cm/hr in multiparous patients
 Etiologies include inadequate uterine activity, cephalopelvic disproportion and fetal malposition
 Methods of evaluating fetopelvic disproportion
o Digital pelvimetry, X-ray pelvimetry, calculation of fetal weight via US
o A C/S is INDICATED if cephalpelvic disproportion is diagnosed.
 Fetal and maternal complications
o Fetal complications incl. shoulder dystocia, internal hydrocephalus, sacrococcygeal teratomas
o Ascites can develop in the mother
 Oxytocin administration
o ACOG recommends the use of oxytocin for ALL protraction and arrest disorders specifically if a DEFINITIVE
diagnosis of prolonged latent phase of labor is occurring or there are other reasons to expedite delivery
o C/I:
 Hyperstimulation  fetal distress from ischemia, rupture of the uterus d/t tetanic contractions
(acts as an ADH giving  severe water intoxication w/convulsions and coma)
 Uterine muscle fatigue and post-delivery uterine atony which increases risks of postpartum
hemorrhage
 Management of abnormal fetal presentations
o For prolonged latent phase:
 Stop sedatives or analgesics and allow self-resolution
 Therapeutic rest with morphine sulfate
 If a DEFINITED diagnosis has been made, augment w/oxytcin
 Amniotomy or artificial rupture of the membranes
o Abnormalities of the active phase:
 Oxytocin use for ALL protraction and arrest disorders
 Indications for VBAC
o If a low transverse cesarean delivery occurred so that the uterine incision did not extend into the cervix or
uterine upper segment
o No history of prior uterine rupture
o Adequate maternal pelvic dimensions

o Success rate is 70%
Emergency management of breech and shoulder dystocia
o Deliver breech via C/S
o Shoulder dystocia occurring during labor should have suprapubic pressure engaged to guide the anterior
shoulder under or away from pubic symphysis
o McRoberts maneuver is having the maternal thighs sharply flexed against the maternal abdomen to reduce
the angle b/w the sacrum and spine  freeing of the impacted shoulder
o If unsuccessful, put a hand in the vagina, grab post. arm and place across chest  delivery of post. shoulder
and displacement of ant. shoulder from pubic symphysis
o If all fails, break the clavicles away from the pleural cavity to prevent traumatic puncture of lungs and pull
Third Trimester Bleeding
 Approach to the patient
o A team approach involving the ob/gyn, anesthesiologist and nurses to establish hemodynamic stability
o At least two large-bore peripheral IV lines should be placed for the most rapid replacement of fluid and
blood volume
o A central line should be placed to manage hypovolemic shock
o Vital signs and amt. of bleeding checked immediately and past medical history for bleeding disorders
o Pelvic exam should NOT be done until placenta previa is EXCLUDED
o Get patient’s coagulation profile by obtaining platelet count, serum firbrinogen level, PT, PTT and type and
cross to have blood on reserve
o To determine cause, an accurate method = US
 Symptoms, physical findings and diagnostic methods
o Placenta previa
 Most common type of abnormal placentation
 Predisposing factors: multiparity, AMA, prior placenta previa and grand multiparity
 PAINLESS vaginal bleeding in a previously normal pregnancy
 Diagnosed via transabdominal US with 95% accuracy
 100% accuracy with TVUS
o Abruption placentae
 Premature separation of the normally implanted placenta
 PAINFUL vaginal bleeding in assoc. with uterine tenderness, hyperactivity and increased tone
 Diagnosis is CLINICAL as US only detects 2%
 Risk factors: crack/coke and tobacco use, maternal HTN, prior placental abruption, polyhydramnios,
folate deficiency
o Uterine rupture
 A prior uterine scar is assoc. with 40% of cases
 Characterized by the sudden onset of intense abdominal pain and some vaginal bleeding
 Complications
o Placenta previa  antepartum or intrapartum hemorrhage, preterm delivery, mal-presentation
o Abruption placentae  perinatal mortality, neurological impairment in the infant, DIC in pregnancy d/t
maternal release of thromoplastin from disrupted placenta, hypovolemic shock and acute renal failure,
Sheehan’s syndrome
 Immediate management of secondary shock
o Two large bore IV needles, type and screen to have multiple units of packed RBCs to restore intravascular
volume
o Resuscitation w/normal saline requires a volume 3X the estimated blood loss
 Blood products and indications for their use
o Platelet concentrate increases platelet count by 20,000-25,000
o Cryoprecipitate supplies fibrinogen, factors VIII and XIII (3-10X more concentrated than the equivalent
volume of fresh plasma)
o FFP supplies all factors EXCEPT platelets
o Packed RBCs raises Hct 3-4%
Preterm Labor
 Predisposing factors:
o multiple gestation, infection (esp. BV), PROM, uterine anomalies, previous preterm labor, polyhydramnios,
abruption placentae, poor maternal nutrition, low SES
o Most patients have NO identifiable risk factors
 S/S of premature uterine contractions
o Menstrual-like cramping, sudden onset of lower back pain, pelvic pressure, vaginal discharge or bleeding,
regular uterine contractions (more than three every 30secs for 30mins)
 Causes
o Infection: cervical pathway, placental-vascular pathway, stress-strain pathway, uterine stretch pathway
 Management
o Assess cervical length/dilatation/station
o Ensure good hydration and bed rest
o Take cultures for GBS
o Administer Abx for ANYONE in preterm labor
 Ampicillin and erythromycin or substitute clindamycin for ampicillin if allergic to PCN
o Labs: CBC, UA, urine culture, electrolytes
o Check fetal status w/US
o If patient does not respond to bed rest and hydration, tocolytics are indicated
 Mg sulfate, nifedipine, prostaglandin synthetase inhibitors (indomethacin)
Premature Rupture of Membranes (PROM)
 History, physical findings and diagnostic methods for confirmation
o Diagnosis is based on the history of vaginal loss of fluid and confirmation of amniotic fluid in the vagina
o Pooling of amniotic fluid in the posterior vaginal fornix can be seen
o Valsalva maneuver or slight fundal pressure may expel fluid from the os = DIAGNOSTIC
o Confirmation:
 Testing the fluid w/nitrazine paper (turns blue w/ basic amniotic fluid)
 Placing a sample of fluid on a slide to look for ferning
 Predisposing factors
o Etiology is unclear
o Risk factors: infection, abnormal membrane physiology, incompetent cervix, nutritional deficiencies
 Expectant management vs. Immediate delivery
o For preterm fetuses, risks associated with preterm delivery must be balanced against the risks for infection
and sepsis
o Risks to mom include chorioamnionitis and the possibility of failed induction due to an unfavorable cervix
o Management is dictated by gestational age at the time of rupture
 Quantity of amniotic fluid may be as important as gestational age in determining outcome
o Oligohydramnios associated with PROM in fetuses ≤24wks  pulmonary hypoplasia
o If PROM occurs ≥36wks and the cervix is favorable, labor should be induced after 6-12hrs if no spontaneous
contractions occur
o Conservative management applies to the care of patients with PPROM who are observed with the
expectation of prolonging gestation
o Risk for infection increases with duration of membrane rupture
o Goal of expectant management is to continue the pregnancy until the lung profile is mature
 Maternal and Fetal Monitoring during Expectant Management
o Applies to patients with PPROM who are observed with the goal of extending gestation
o Goal is to continue until the lungs are mature
o Careful surveillance via mother’s temp. and gram stain for chorioamnionitis is indicated


A tender uterus, temp. >100.4F, bacteria on gram stain and utertine irritability on NST are
indicative of chrioamnionisits
o Ampicillin or erythromycin significantly prolongs the interval to delivery
Outcome when PROM occurs preterm
o Depends on the lung profile
o If L/S ratio >2, there is little risk of RDS
o If L/s <2 and no PG is present, >90% of neonates develop RDS
o Decreased amniotic fluid  cord compression and variable decels  C/S
Post Term Pregnancy
 Normal period of gestation: 37-42wks
 Complications of post-maturity
o Perinatal mortality is 2-3X higher
o Fetal dysmaturity syndrome can happen (due to aging placenta), IUGR, macrosomia, anencephaly
 Management of Prolonged Gestation
o Revolves around identification of the low percentage of fetuses with post-maturity syndrome who are
truly at risk for hypoxia and fetal demise
o If the EGA is 42wks, head is well fixed in the pelvis and the cervix if favorable, labor should be induced
o If the cervix isn’t ripe, bi-weekly NSTs should be taken + BPP performed with AFI
 If AFI <5 (oligohydramnios) or if spontaneous fetal HR decels, delivery is indicated
o Usually at 42 weeks, delivery is indicated
o Continuous fetal monitoring should be employed during induction and membranes ruptured as early as
feasible
o C/S is indicated for fetal distress
Fetal Growth Abnormalities
 Macrosonmia – a birth weight >4000g (or 4500g???)
 IUGR is defined when the birth weight of a newborn infant is below the 10th percentile for a given gestational
age
 Etiologies of abnormal growth
o Maternal
 Poor nutritional intake, cigarette smoking, drug abuse, alcoholism, cyanotic heart disease,
pulmonary hypertension and antiphospholipid syndrome
o Placental
 Inadequate substrate transfer b/c of placental insufficiency
 Caused by essential HTN, chronic renal disease and pregnancy-induced HTN
o Fetal
 Inadequate substrate (Ex. – intrauterine infection (listeria and TORCH) and congenital
abnormalities)
 Etiologies of macrosomia
o Associated with post-term pregnancy, maternal DM, pre-pregnancy weight, weight gain during
pregnancy, multiparity, male sex, gestational age >40wks, ethnicity, maternal birth weight, maternal
height and maternal age
 Methods of Detection
o IUGR
 Serial uterine fundal height measurements = primary screening tool


Sonographic assessment if fundal height lags >3cm behind a well-established gestational age or
the mother has a high risk condition such (pre-existing HTN, chronic renal disease, DM, pre-E,
viral disease, drug addiction or lupus/antiphospholipid Abs)
o For macrosomia
 US, but only 50% accurate
Morbidity and Mortality
o IUGR
 Infants are at higher risk for adult onset DM, HTN and atherosclerosis
 Good prognosis if IUGR is not from chromosomal abnormalities, autoimmune disease,
congenital anomalies or infection
o Macrosomia
 Maternal morbidity associated with macrosomia includes labor dystocia, shoulder dystocia, and
genital trauma
 Increased risk of postpartum hemorrhage and puerperal infection
 Neonatal problems include Erb’s palsy and Klumpke’s palsy
Obstetric Procedures
 Ultrasound
o Can be done transvaginal or transabdominal
o Indications
 Transvaginal
 Useful in the first trimester of pregnancy to determine accurate dating of the
pregnancy as well as fetal location and number
 Can also do nuchal translucency measurement between weeks 11 and 14
 Can check cervical length in the second trimester for risk of preterm labor
 Used in the second and third trimester for location of the placenta in relation to the
internal os
 Transabdominal
 Used after 16wks to evaluate structural abnormalities, provide baseline assessment of
fetal growth and provide information regarding fetal well-being
o No complications
 Chorionic villous sampling
o Performed in the 10-12wk period
o Can go transcervical or transabdominal with a syringe into the placenta for fragments of placental villi
o Indications
 Access fetal cells for prenatal genetic diagnosis
o Complications
 Procedure related loss rate is <1%
 Rho-GAM should be administered to Rh- patients
 Amniocentesis and cordocentesis
o Involves removing a sample of fluid from the amniotic cavity
o Use direct ultrasonic guidance to guide 22g needle into a pocket of amniotic fluid
 Give Rho-GAM to those who are Rho Indications
 Done 16-20wks to diagnosis chromosomal anomalies
 Can get AFP levels and check for perinatal infections (CMV)
 To check for lung maturity in the 3rd trimester







 To drain XS amniotic fluid in polyhydramnios
o Complications
 0.3% pregnancy loss rate and 1% post-procedure measurable amniotic fluid leakage rate
Antepartum fetal assessment
o Biophysical profile, amniocentesis, CVS, NST, US
Intrapartum fetal surveillance
o Auscultation of fetal heart rate, continuous electronic fetal monitoring (acceleration vs deceleration),
umbilical cord blood sampling
Induction and augmentation of labor
o Induction is the process whereby labor is initiated by artifical means
o Augmentation is the artificial stimulation of labor that has already begun spontaneously
o Can give local PGs for cervical ripening, artifical rupture of the membranes, or oxytocin/pitocin
o Indications
 Absence of natural onset of labor
o Complications
 Oxytocin can cause hyperstimiulation  fetal distress if infusion rate is too fast
 Rupture of the uterus, water intoxication from antidiuretic effect, uterine muscle fatigue and
post-delivery atony
Episiotomy
o Mediolateral or midline vaginal incision into the perineal tissue
o Indications
 Reduce perineal resistance to the baby coming out
 Current management is to allow the fetus to deliver without an episiotomy
o Complications
 Bleeding, infection, further tearing of tissue
Spontaneous vaginal delivery
o Baby comes out of the vagina spontaneously
o Indications: vertex position
o Complications
 Shoulder dystocia, perineal tear, hemorrhage
Vacuum-assisted delivery
o Suction cup applied to the fetal head
o Flexion of the fetal head must be maintained to provide the smallest diameter to the maternal pelvis
o Posterior edge of the suction cup is placed 3cm from the anterior fontanelle squarely over the sagittal
suture
o Indications
 Prolonged second stage of labor, suspicion of immediate or impending fetal compromise, to
stabilize the aftercoming head during a breech delivery, to shorten the second stage of labor,
maternal benefit
o Complications: cephalohematomas, subgaleal hematomas
Forceps delivery
o Using instruments designed to provide traction and rotation of the fetal head when the explusive
efforts of the mother are insufficient to accomplish safe delivery of the fetus
o Indications
 Prolonged second stage of labor, suspicion of immediate or impending fetal compromise, to
stabilize the aftercoming head during a breech delivery, to shorten the second stage of labor,
maternal benefit
o



Complications
 Increased risk for trauma to the vaginal and perineal tissue, damage to maternal anal sphincter
Breech delivery
o Description – fetus is coming out feet first instead of head first
o Indications – need to do a c-section if cant get fetus in vertex position
o Complications – see c-section
Cesarean delivery
o Delivery of fetus through an incision in the maternal abdomen and uterus
o Indications
 Dystocia, repeat cesarean, breech presentation, fetal distress
 An ABSOLUTE indication is a previous full-thickness, non-transverse incision through the
myometrium
o Complications
 Uterine rupture, hemorrhage, postpartum infection, thromboembolism
Vaginal delivery after Cesarean section (VBAC)
o Indications
 Can do this after one C/S
 Risk of uterine rupture = 3%
 Will NOT be done after two C/S
o Complications: uterine rupture
Menstrual Cycle and Vaginal Bleeding
 Abnormal Bleeding
o Normal menstrual cycle
 Normal ovulatory cycle (28 days) can be divided into a follicular and luteal phase
 The follicular phase begins with the onset of menses and ends in the pre-ovulatory surge of LH
 The luteal phase begins with the onset of the pre-ovulatory LH surge and ends with the first
days of menses
o Abnormal uterine bleeding vs. dysfunctional uterine bleeding
 Dysfunctional uterine bleeding is defined as abnormal uterine bleeding in women between
menarche and menopause that cannot be attributed to medications, blood dyscrasias, systemic
diseases, trauma, uterine neoplasms or pregnancy
 This form of AUB is almost always caused by aberrations in the hypothalamic-pituitaryovarian hormonal axis  anovulation
 The diagnosis of DUB is made by excluding other treatable causes of AUB
o Causes of abnormal uterine bleeding
 Iatrogenic
 Exogenous estrogen, aspirin, heparin, sodium warfarin, tamoxifen, IUDs
 Dyscrasias
 Thrombocytopenia, increased fibrinolysins, autoimmune disease, leukemia, vWD
 Systemic disorders
 Hepatic disease, renal disease, thyroid disease
 Trauma
 Laceration, abrasion, foreign body
 Organic Conditions
 Complication of pregnancy, uterine leiomyomas, malignancies of cervix or corpus,
endometrial polyp, adenomyosis, endometritis, endometrial hyperplasia
o

Evaluation/Diagnosis of AUB
 A possible unexpected pregnancy should always be ruled out
 Laboratory evaluation
 CBC, platelet count, serum iron and iron-binding globulin, coagulation studies, bleeding
time, urinary hCG, thyroid function studies, serum progesterone, LFTs, prolactin levels,
serum FSH
 Diagnostic procedures
 Cervical cytology, endometrial biopsy, pipelle, office curette, vacuum curette, pelvic US,
hysteroscopy/hysterosonogram, D&C
o Therapeutic options
 Observation and expectant management for less significant bleeding
 Heavy endometrial hemorrhage from menarche through peri-menopause may require high
dose estrogens to support the endometrium and diminish bleeding
 If the bleeding slows down, lower dose oral estrogen followed by or in combination with
progestin can then be initiated
 If the bleeding is unremitting, D&C may be necessary
 More common/less urgent type of DUB is best managed by cyclic estrogens with a progestin
added in the latter 10-15d of the 25d estrogen cycle
 Cyclic progestins alone may be used for younger patients who are likely to have sufficient
endogenous estrogens to prime endometrial progesterone receptors
 For older patients who do not respond to medical therapy and who do not anticipate later
pregnancies, endometrial ablation and hysterectomy may be considered
Leiomyomas
o Prevalence of uterine leiomyomas
 Most common neoplasm of the uterus
 Primary indication for hysterectomy in the US each year
o Symptoms and physical findings
 Most uterine leiomyomas cause no symptoms
 Women may complain of lower abdominal mass, pelvic pressure, congestion, bloating, a feeling
of heaviness in the lower abdomen or lower back pain
 Frequency of urination if it presses on the bladder
 Prolonged or heavy menstrual bleeding may be associated with intramural or submucosal
myoma
 Intermenstrual bleeding is NOT characteristic of these tumors
 Fibroids are not generally painful, but severe pain can be associated with red degeneration
(acute infarction) within a fibroid
 Increased incidence of secondary dysmenorrhea
 Submucosal leiomyomas may be associated with increased incidence of infertility
o Confirmation of diagnosis
 US may visualize the fibroids and identify normal ovaries vs. leiomyomas
o Indications for medical and surgical treatment
 If a small, asymptomatic fibroid is detected, treatment is not necessary
 Unless the fibroid uterus is excessively large or is implicated as a cause of infertility in a women
seeking pregnancy, the first line of treatment is targeted to her symptoms
 Goal is to reduce monthly menstrual blood loss with cyclic hormonal methods or to eliminate
menses with extended or continuous use of these methods




Can use GnRH agonists and possibly the selective anti-progesterone receptor antagonist
mifepristone
For women desiring to preserve their fertility, myomectomy may be an option
 The surgical approach depends on the location of the myoma
Amenorrhea
o Primary amenorrhea
 Diagnosis is made when no spontaneous uterine bleeding has occurred by the age of 16
o Secondary amenorrhea
 Menses has been absent for ≥6mos
o Oligoamenorrhea
 Menstrual cycles >35-45d intervals
o Causes
 Most common causes = pregnancy and menopause
 Primary amenorrhea with sexual infantilism
 Hypogonadrotropic hypogonadism, hypergonadotropic hypogonadism, 17-hydroxylase
deficiency
 Primary amenorrhea with breast development and mullerian anomalies
 AIS (46XY), normal female karyotype (46XX), transverse vaginal septum, cervical
agensis, mullerian agenesis/dysgenesis
 Amenorrhea/oligomenorrhea with breast development and normal mullerian structures
 Pregnancy, uterine defects, hypoestrogenism, hypopituitary dysfunction, premature
ovarian failure, hyperprolactinemia, normal estrogen and amenorrhea,
hyperandrogenism
o Methods of evaluation
 Work-up should be initiated earlier than 16yo if there is no evidence of breast development
by 14yo or if the patient has failed to menstruate spontaneously within 2yrs of breast
development
 Presence of normal breast development confirms gonadal secretion of estrogen but not
necessarily the presence of ovarian tissue
 Presence of normal amounts of pubic and axillary hair confirms gonadal or adrenal secretion of
androgens + presence of functional androgen receptors
o Treatment options incl. management of the underlying condition
Premenstrual Syndrome (PMS)
o In both PMS and PMDD, patients experience adverse physical, psychological and behavioral symptoms
during the LUTEAL phase of the menstrual cycle
o Symptoms: depressed mood, anxiety, affective lability and irritability, decreased interest in regular
activity, difficulty concentrating, fatigue, change of appetite, sleep disturbance and feelings of being
overwhelmed
o Theories of etiology
 Arises in part from atypical metabolism of progesterone that results in lower levels of the
steroid allopregnenolone within the CNS
 Allopregnenolone is a neuroactive progesterone metabolite that modulates GABA
receptors that modify behavior, emotion, subjective perceptions and response to stress
o Methods of diagnosis
 Symptoms seriously interfere with usual functioning and relationships
 Premenstrual timing is confirmed by menstrual calendar in two consecutive cycles

o
Symptoms resolve after the onset of menses, are not an exacerbation of another disorder and
have at least five menstrual symptoms:
 One of the following: depressed mood, marked anxiety, marked irritability
 Other possible symptoms: decreased interest in regular activities, difficulty concentrating,
lethargy/fatigue, appetite change/food cravings, sleep disturbance, feelings of being
overwhelmed, physical symptoms (breast swelling and tenderness, bloating, weight gain,
edema or headache)
Management Strategies
 Treat individually and conservatively with reassurance and mild diuretics for symptoms such as
bloating
 Mild anxiety may be treated with antianxiety agents such as buspirinone
 The most effective therapy is the SSRI class of antidepressants: fluoxetine and sertraline
 Benefit from the continuous use or 24/28d use of an OCP containing the progestin
drospirenone.
Contraception and Sterilization
 Physiologic and pharmacologic basis of action
o Primary action of virtually all methods of birth control is contraception (the prevention of fertilization)
o Implant releases etonogestrel at levels adequate to suppress ovulation
o Copper IUD immobilizes and killis
o LNG-IUS (Mirena) thickens mucus to prevent sperm entry
o Combined hormonal products, progestin-only injections and OCPs:
 Thicken cervical mucus and block LH surge to prevent ovulation
o Barrier methods = condoms, diaphragms, vaginal shield, cervical cap, spermicides
o Behavioral methods = withdrawal, lactation, amenorrhea, fertility awareness
o Sterilization = vasectomy (interruption of vas deferens), fallopian tube procedures
 Effectiveness
o IUDs and progestin implants provide the HIGHEST level of pregnancy protection
 1st-year failure rates <1%
o Other hormonal methods have the potential for very low pregnancy rates (1%), but typical use gives
them a failure rate of 7-8%
o For barrier and behavioral methods, the differential between the potential that the method offers and
what is really seen is WIDEST
 Male condoms have <2% failure rate if used correctly and consistently, but in real life the
failure rate is 17.4%
 Female barrier methods have higher pregnancy rates
o Behavioral methods are almost equivalent to any barrier methods
 The most effective behavioral method is withdrawal
 Risks and benefits
o Tier 1 (implants, IUDs)
 Most effective option, reversible, very safe and can be used by women with serious medical
conditions for whom pregnancy may be very dangerous
 Implant allows fertility soon after removal and can cause irregular bleeding
 Copper IUD is rapidly reversible, good for 10yrs but can cause heavy/painful menses
 Mirena is rapidly reversible, good for 5yrs and can make periods lighter
o Tier 2 (other hormonal methods)
 Combined hormonal products


Benefits: regulation of menstrual cycle, lighter/shorter periods, treatment of acne,
treatment of PMDD, decreased risk of ovarian cancer
 Risks: increased incidence of venous TE, benign hepatic tumors, symptomatic
cholelithiasis, mild HTN
 Contraindications: history of heart attack, stroke, breast cancer, labile HTN, advanced
diabetes, hepatic failure, migraine with aura, unexplained abnormal uterine bleeding
 Progestin-only pills and Injections
 Progestin only pills are immediately reversible
 Reversal of Depo shot takes a median time of 10mos
 Depo shot can cause weight gain but benefits include amenorrhea, reduced incidence
of menorrhagia/dysmenorrheal/pain from endometriosis/endometrial cancer/acute
sickle cell crisis
 Barrier and behavioral methods
 Advantage = only need to be used at time of intercourse but this increases failure rate
 Condoms prevent STIs
 Sterilization
 Reversibility may or may not be an option
 Methods are less effective in younger women
 Long-term complication rates are low but many women have regrets
Financial considerations
o Copper IUD = most cost effective method over time
Vulvar and Vaginal Disease
 Normal vagina
o Non-keratinized stratified squamous epithelium
o Newborn vagina is colonized by aerobic and anaerobic bacteria acquired while passing through the
birth canal
o It is strongly estrogenized and rich in glycogen supporting growth of lactobacilli
o Mucus secretions are composed of proteins, polysacchs, AA’s, enzymes and Igs
 Evaluation of Vaginitis
o BV: clue cells in a wet prep, +whiff test with KOH and vaginal pH >4.5
o Candida: wet prep/KOH showing pseudohyphae
o Trich: motile trichomonads on wet mount
 Management of Vaginitis
o Metronidazole for BV and Trich
o Butoconazole or fluconazole for candidiasis
 Common vulvar problems
o Atrophic vaginitis
 Immature basal cells and parabasal cells replacing superficial vaginal epithelial cells on Pap
smear
 Manage with topical estrogen (Premarin)
o Vulvodynia
 A diagnosis of EXCLUSION
 Managed via removal of all irritants, low dose trial of TCA’s, gabapentin-carbamazepine,
capsaician creams
o Bartholin’s Gland Disease
 Look at the base of cyst and rule out Bartholin’s carcinoma
o
 Drainage
Trauma
 Usually d/t sexual assault or tampons
Sexually Transmitted Infections
 Syphilis
o Diagnosed with FTA-ABS but screening includes VDRL or a rapid plasma regain test (RPR)
o S/S: painless chancre, rash on hands and feet, neuro or cardiac signs (tertiary)
 Herpes Simplex Virus (HSV)
o Silent when the virus is dormant or recurrence occurs
o Usual clinical presentation is of multiple, bilateral and PAINFUL anogenital vesicles or ulcers with an
erythematous base,
 Fever, headache, malaise and LAD may also be present
o To confirm, viral culture of live lesion cells, PCR, or type-specific serologic tests for HSV-1 and HSV-2
antibodies
 Gonorrhea
o Most women are asymptomatic
o Swollen, red cervix and mucopurulent discharge, acute urethritis
o Diagnose via gram stain of cervical discharge, culture on Thayer-martin media, DNA hybridization test
 Chlamydia
o Highest incidence in USA
o No symptoms in 70% but 30% have mucopurulent discharge and acute urethritis with dysuria
o Diagnose via lab cultures, antigen tests, DNA hybridization tests
Pelvic Inflammatory Disease
 Pathogenesis of salpingitis
o From untreated chlamydia, gonorrhea and genital mycoplasmas
 S/S
o Low abdominal pain and tenderness, vaginal discharge, N/V, uterine and adnexal tenderness,
mucopurulent cervicitis
 Management
o Improve symptoms, prevent long-term sequelae and eradicate causal agents from both the patient and
her sexual partner
o Abx such as ceftriaxone and doxy
o Counsel the patient about STIs, prevention and immunizations and partner evaluation/treatment
o Routine screens, treat with a single dose of azithromycin, including all partners within the last 60d
 Long-term sequelae
o Increased risk for premature labor, tubo-ovarian abscess and chronic salpingitis
o 6x more likely to have ectopic PGs
o 14x more likely to have tubal infertility
o 6-10x more likely to have endometriosis, suffer from CPP, require a hysterectomy
Cervical Dysplasia
 Epidemiology and clinical burden of HPV
o 75% of sexually active adults will be infected sometime in their lifetime by HPV
o Some subtypes are strongly assoc. with cervical cancer
o





Young cervices are more susceptible to carcinogenic stimuli b/c of the active process of squamous
metaplasia, which occurs within the transformation zone during periods of endocrine change
Risk factors for cervical and vulvar neoplasia and cancer
o Young, poor women with multiple sexual partners who smoke, young age at first PG, high parity
Indications for screening
o Screen with annual Pap all women within 3yrs of sexual intercourse or by age 21
o Annual screening until age 30, then every 2-3yrs afterward
o Sample BOTH endo and ectocervices during Pap smear on Thin Prep
o Screen even if she has been vaccinated with Gardasil
Appropriate utilization of new techniques for evaluating cervical neoplasia
o Cost effectiveness of HPV DNA testing s currently under investigation
 More sensitive than cervical cytology but less specific
Technique for obtaining an adequate Pap smear
o Need a sample from the transformation zone to see the metaplastic squamous epithelium located b/w
the original and new SCJ
Management of an abnormal Pap smear
o Punch biopsy (colpo)
o Manage patients with cryotherapy, large loop excision of transformation zone, radical surgery if
invasive, hysterectomy
Pelvic Pain
 Endometriosis and Dysmenorrhea
o Premenstrual Syndrome (PMS)
 Occurs in 80% of regularly ovulating women
 Includes symptoms of depressed mood, anxiety, affective lability and irritability, decreased
interest in regular activity, fatigue, difficulty concentrating, sleep and appetite changes,
overwhelmed
 Theories of etiology
 Arises from atypical metabolism of progesterone  low levels of pregnenolone within
CNS which normally modulates GABA receptors
 Methods of diagnosis
 Symptoms interfere with usual functioning of relationships
 Premenstrual timing is confirmed by menstrual calendar in two consecutive cycles
 Symptoms resolve after onset of menses and they are not an exacerbation of another
disorder
 Patient has at least 5 premenstrual symptoms (listed above)
 Management strategies
 Treat with reassurance, diuretics for bloating, buspirone for anxiety,
fluoxetine/setraline for depression, GnRH agonists for hot flashes
o Primary Dysmenorrhea
 Occurs during ovulatory cycles and appears within 6-12mos of menarche
 No identifiable cause but evidence that it occurs in women with higher PG
 Assoc. with younger women
o Secondary dysmenorrhea is d/t organic pelvic disease
 Causes include endometriosis, pelvic inflammation, adenomyosis, firbroid tumors, ovarian
cysts, pelvic congestion
 Seen more commonly in older women
o

Management strategies
 Primary dysmenorrhea
 NSAIDS (COX inhibitors of the PGs) such as ibuprofen, naproxen
 OCPs, patches or vaginal rings to reduce menstrual flow and inhibit ovulation
 Resistant cases can be treated with salbutamol, nifedipine.
 For secondary dysmenorrhea, treatment of the underlying disease is recommended
Chronic Pelvic Pain
o Pain of more than 6mos duration that has significant effect on daily function and quality of life
o Etiology
 Endometriosis, chronic PID, ovarian remnant syndrome (from previous surgeries), pelvic
congestion syndrome (women with pelvic vein varicosities and congested pelvic organs)
 GI problems (IBS, partial bowel obstruction, IBD, diverticulitis, hernias)
 Degenerating uterine fibroid, adenomyosis, adhesions.
o Diagnostic procedures
 Dependent upon the etiology
 Pelvic US, abdominal and pelvic CT, endoscopy, cystoscopy, lumbosacral X-ray, MRI.
 Diagnostic laparoscopy is the ULTIMATE method of diagnosis for patients with CPP of
undetermined etiology
o Management options
 Symptomatic therapy
 MOST IMPORTANT = referral to a multidisciplinary pain clinic or creation of one within a
specific practice setting
 Relaxation, cognitive and behavioral therapies are employed to replace the pain behavior
 Multidisciplinary management has been shown to be more effective than traditional
gynecological management
Breast Disorders
 Breast Exam
o Self-exam
 Should be done every menstrual period
 Woman should be upright, carefully inspecting with arms initially by her sides and then above
her head
 Palpate the supraclavicular and axillary regions for node enlargement
 Lie down and palpate each quadrant using the flat of her fingers
 Finally, she should palpate the areolar areas and compress nipples looking for secretion
o Physician Exam
 Should be done annually
 Inspect breasts in an upright position observing contour and symmetry and note any skin
changes or nipple retraction
 Skin retraction may be highlighted by having the patient extend arms over head
 Palpation of the breast, areola, and nipple is performed with the flat of the hand
 If any mass is palpated, ask the patient to place her hands over her hips and contract her pecs
 Each axilla is then examined while the patient’s arm is supported
 Palpate the supraclavicular fossa
 After palpation in the upright position, the exam is repeated lying down
 On mammography, densities and fine calcifications are suspicious findings and clinically
unapparent malignancies <1cm may be detected







89% of most breast cancers were shown by mammography, 42% percent of which were not
clinically evident.
Approach to a woman with CC of breast mass, nipple discharge or breast pain
o Definitive diagnosis may be with open biopsy or FNA cytology
o For FNA, a negative result should never be accepted as definitive when there are clinical or
mammographic indications that the lesion may be malignant
o In the presence of a palpable lump, FNA should make it possible to diagnose breast cancer without
formal excisional biopsy 90% of the time
o ABSOLUTE indications for open breast biopsy:
 A clinically suspicious mass that persists through a menstrual cycle, regardless of
mammographic findings
 A cystic mass that is bloody or does not completely collapse on aspiration, spontaneous serous
or serousanguinous nipple discharge in the absence of a mass
Intraductal papilloma
o Papillary neoplastic growths may develop within the ducts of the breast
o Most commonly just before or during menopause
o Rarely palpable and usually diagnosed because of bloody, serous, or turbid discharge
o Mammography and cytologic exam of fluid are helpful
o Excisional biopsy is treatment
Fibrocystic changes
o 3 categories:
 Non-proliferative lesions, hyperplasia without atypia and atypical hyperplasia
o Hyperplasia is the most common benign breast disorder
 May involve any or all breast tissues
 When associated with atypia, there is an increase in possible malignant changes
 Due to a decrease in progesterone and increase in estrogen???
 Usually happens in premenopausal years and improves with pregnancy
 The lesions are usually multiple, bilateral, painful and tender (premenstrually)
Fibradenoma
o Composed of both fibrous and glandular tissue
o Most common BENIGN tumor of female breasts
o Sharply circumscribed and freely mobile, usually solitary
o Occurs at any age but usually before 30
o Pregnancy accelerates growth
o Menopause causes regression and calcification
Carcinoma
o About 80% of all breast cancers are infiltrating ductal carcinomas
o Usually a significant fibrotic response, stony hard on palpation
o Usually painless but a serous or bloody nipple discharge may be present
o With growth it may become affixed to fascia  retraction and dimpling
Mastitis
o An uncommon complication with breastfeeding
o Slight fever and chills, redness of a segment of the breast which becomes indurated and painful
o Usually S. aureus and treated with dicloxacillin
o Continue breastfeeding to drain the area
Infertility





Primary – occurs without any prior pregnancy
Secondary – following a previous conception
Male Infertility
o Low sperm count, ≥35yo, smoking tobacco, abusing alcohol, using certain illegal drugs
o Overweight/ underweight, having certain past or present infections
o Toxin exposure, testicular over-heating,
o Prior vasectomy or vasectomy reversal, being born with a fertility disorder or having a blood relative
with a fertility disorder,
o Certain medical conditions including tumors and chronic illnesses
o Medication, surgery or radiation, bicycling for prolonged periods, especially on a hard seat or poorly
adjusted bicycle
Female Infertility
o Ovulation problems, >32yo, smoking, obesity, pelvic anomalies, STDs, EtOH and caffeine, endometriosis
Evaluation and management
o The first 6-8mos of evaluation involve simple and noninvasive tests and the performance of a radiologic
evaluation of tubal patency (HSG)
o Operative evaluation by laparoscopy is reserved for those females who haven’t conceived after 1824mos
o A semen analysis should be performed following a 2-4day period of abstinence
o The couple should be advised to have sex every 1-2d during the periovulatory period
o The woman should be advised to lay on her back for 15mins after coitus
o Smoking should be stopped
o Men should not use saunas, hot tubs, or tight underwear
o Treat with IUI if sperm volume is low
o Try hMG injections if low sperm density/motility
o For women, try clomiphene if ovulation not abnormal
o Try hMG or pulsatile GnRH for pituitary insufficiency
o Clomiphene for PCOS
o Microsurgical tuboplasty for tubal problems
o Laparoscopic lysing of adhesions or removal of endometriosis for peritoneal problems
o IVF
Pelvic Relaxation and Urincary Incontinence
 Cystocele
o Anterior vaginal prolapse
o Most common site of prolapsed
o Women describe vaginal fullness, heaviness, pressure and discomfort
o May have to apply manual pressure to empty their bladder fully
o Other symptoms include stress incontinence, urgency, frequency, nocturia
o Significant prolapse  urethral kinking
 Rectocele
o Posterior vaginal prolapse
o Weakness in the rectovaginal septum
o Symptoms: discomfort, pressure, sense of vaginal bulge, problems with bowel function
o Straining or need to splint for bowel evacuation
o If it has loops of bowel = enterocele




Vaginal vault/prolapse
o Eversion of the vagina may be seen after vaginal or abdominal hysterectomy and represents failure of
the supports around the upper vagina
Methods to treat incontinence and POP
o Kegel exercises to strengthen the pelvic floor
o Pessaries and estrogen therapy for SUI
o Surgical
 SUI: abdominal retropubic urethropexy/suburethral sling/TVT
 Urge incontinence:
 Reduce fluid intake/avoid liquids during the evening hours
 Kegel exercises
 Anti-muscarinics like oxybutinin, trospium, tolteridone, imipramine
 POP:
 Anterior/posterior colporrhaphy/colpopexy (for apical prolapsed)
 Lefort colpocleisis is an option for women who no longer desire coitus
 Prolift anterior and posterior repairs
Screening questions for urinary incontinence
o Do you leak urine when you cough, laugh, lift something or sneeze?
o Do you ever leak urine when you have a strong urge on the way to the bathroom?
o How frequently do you empty your bladder during the day?
o How many times do you get up to urinate after going to sleep? Is it the urge to urinate that wakes you?
o Do ever leak urine during sex?
o Do you wear pads that protect you from leaking urine? If so, how often do you have to change them?
o Do you ever find urine on your pads or clothes and were unaware of when the leakage occurred?
o Does it hurt when you urinate? Do you ever feel that you are unable to completely empty your
bladder?
Incontinence
o Stress incontinence
 The involuntary loss of urine during an increase of intra-abdominal pressure produced from
activities such as coughing, laughing or exercising
 The underlying abnormality is typically urethral hypermobility caused by a failure of the normal
anatomic supports of the urethrovesical junction (bladder neck)
o Urge incontinence
 Involuntary loss of urine preceded by a strong urge to void, whether or not the bladder is full
 The (FDA) adopted the term "overactive bladder" to describe a clinical syndrome that includes
not only urge incontinence, but urgency, frequency, dysuria and nocturia
 Other commonly used terms such as detrusor instability and detrusor hyper-reflexia refer to
involuntary detrusor contractions observed during urodynamic studies.
o Overflow incontinence
 Urine loss associated with over-distension of the bladder
 Patients can present with frequent or constant dribbling, overactive bladder or stress
incontinence
 Over-distension is typically caused by an underactive bladder (detrusor) muscle and/or outlet
obstruction
 The detrusor muscle may be underactive secondary to drug therapy (esp. from psychotropic
medications) or conditions such as diabetic neuropathy, low s.c. injury, radical pelvic surgery
and MS

Outlet obstruction in women is almost always a result of urethral occlusion from pelvic organ
prolapse or previous anti-incontinence surgery
Menopause/Climacteric
 Physio. changes in the hypothalamic-pituitary-ovarian axis assoc. with perimenopause / menopause
o Ovaries begin to fail
o Estradiol values decline, decrease in the level of circulating androgens
o Progesterone decreases
o GnRH increases  increases in LH and FSH
o Typical levels of FSH in postmenopausal women are >20-40 IU/L
 Management of menopausal /peri-menopausal symptoms
o Osteoporosis
 Consume 1200-1500mg of calcium and 400-600U of VitD daily
 Encourage walking and weight bearing exercises
 Pharmacological treatments such as estrogen, SERMs, bisphosphonates, calcitonin, PTH
o For women that still have a uterus – give continuous COMBINED estrogen and progestin
 Do not give unopposed estrogen!
o If patient’s main concerns are with genitourinary symptoms, vaginal estrogen cream, tablets or rings
may be used on an as-needed basis
o Counsel patients regarding menopausal issues
 Long-term changes associated with menopause
o Osteoporosis
o Dementia of the alzheimer’s type (possible)
o CV disease & cancer (unclear relationship)
Abortion



Surgical and non-surgical pregnancy termination methods
o Mifepristone (an anti-progestin) can be administered and followed later by misoprostol (a
prostaglandin) to induce uterine contractions and expulsion of the products of conception
o Methotrexate can also be used but has been found to not be as effective
o Aspiration with a manual vacuum or section curettage after cervical dilation with misoprostol or
laminaria
Complications
o Hemorrhage, infection, uterine perforation, retained products of conception and anesthetic
complications
Psychosocial considerations
o Have to worry about how the mother will feel after the procedure is done
o Have to make sure the mother the procedure and is psychologically prepared for it
Hirsutism and Virilization
 Hirsutism
o The presence of male-like hair growth caused by conversion of vellus to terminal hairs in areas such as
the face, chest, abdomen, or upper thighs
 Virilization
o The addition of temporal balding, deepening of the voice and enlargement of the clitoris
 Causes
o Ovarian


PCOS (hyperandrogenism of PCOS results from an overproduction of male hormones by the
ovary and also from the adrenal gland)
Neoplasms

o Adrenal
 CAH (most common is 21-hydroxylase deficiency)
 Adrenal enzyme deficiency associated with the overproduction of steroids
 21-hydroxylase deficiency  increased 17-hydroxyprogesterone which can be used a
marker for the disease
 Cushing syndrome from a cortisol producing tumor of the adrenal gland, adrenal neoplasm
o Pituitary
 ATCH-producing pituitary adenoma (Cushing’s disease)
o Pharmacological
 Cushing syndrome from taking steroids and not tapering them off
Hyperandrogenic insulin resistance and acanthosis nigricans
o Characterized by extremely high circulating levels of insulin due to severe insulin resistance
Gynecology Oncology
 Vaginal / Vulvar Cancer
o Risk factors for vulvar neoplasms
 One type seen mainly in younger patients is related to HPV infection and smoking and is
commonly associated with VIN of the basaloid or warty type
 The more common type is seen mainly in elderly women and is unrelated to smoking or HPV
 Long-standing lichen sclerosus is common
 When VIN is present, it is of the differentiated type
 VINIII carries a significant risk for progression to invasive cancer if left untreated
 5% of patients have positive results on testing for syphilis
 Vulvar cancer occurs in assoc. with lymphogranuloma venereum and granuloma inguinale
o Methods of diagnosis
 Careful inspection of the vulva in a bright light, with the aid of a magnifying glass if necessary
 Any pigmented lesion on the vulva requires excisional biopsy for histologic diagnosis
o Management
 Mainstay of treatment for intraepithelial neoplasia = local superficial surgical excision with
primary closure
 SCC
 A conservative approach for the primary lesion and groin dissection through a separate
groin incision
 Early vulvar cancer requires a wide and deep, local excision
 Advanced vulvar cancer
 Preoperative radiation or chemoradiation should be used to shrink the primary tumor
followed by conservative surgical excision and bowel or urinary stoma
 Malignant melanoma
 Radical local excision of the primary tumor combined with at least ipsilateral inguinal
femoral LAD
 Verrucous carcinoma requires surgical excision as radiation is CONTRAINDICATED!!!
 Bartholin’s gland carcinoma requires hemivulvectomy and ipsilateral inguinofemoral LAD
 Basal cell carcinoma requires a wide, local excision
 Endometrial Carcinoma
o

Risk factors
 Obesity, nulliparity, late menopause, DM, HTN, family history of breast,colon or ovarian cancer
(HPNCC syndrome), chronic unopposed estrogen stimulation, chronic tamoxifen use
o Symptoms
 Most common = abnormal vaginal bleeding
 Postmenopausal bleeding is ALWAYS abnormal and must be investigated
 Signs on pelvic exam of external genitalia are usually normal, but a widely spread apart
(patulous) cervical os or a firm, expanded cervix may indicate extension of disease from the
corpus
 The uterus may be enlarged
o Screening & diagnosis via TVUS
 If endometrial thickness >5mm, endometrial evaluation via biopsy is necessary
 If the endometrial biopsy is negative for cancer or reveals hyperplasia, a hysteroscopy and
fractional D&C should be performed
o Management
 Stage I
 Exploratory laparatomy with TAH + BL salpingo-oophorectomy, unless there are
absolute medical contraindications
 Radiation therapy only on patients with high grade carcinomas
 Hormone therapy w/medroxyprogesterone acetate for 3-6 mos will reverse changes in
2/3 of patients
 Chemotherapy for advanced cancer and recurrent cases
 Stage II
 Regardless of the size, primary radical hysterectomy and BL oophorectomy with pelvic
and para-aortic LAD
 For advanced disease, take everything out (uterus, tubes, ovaries, omental “cake” if
causing abdominal discomfort and ascites
o Prognosis
 Serous and clear cell endometrial carcinomas have a bad prognosis and both are prone to early
dissemination (5yr survival rates are <50%, even for stage I patients )
 Most commonly, 75% of cancers are endometrioid adenocarcinomas
Ovarian Neoplasms
o Evaluation of the patient with an adnexal mass
 A vaginal and rectal exam should be conducted
 A solid, irregular, fixed pelvic mass is suggestive of ovarian cancer
 If combined with an upper abdominal mass, ascites, or both, the diagnosis is almost
certain
 Routine labs and chest radiograph should be taken
 Endometrial biopsy and endocervical curettage should be done because concurrent primary
tumors may occur in the ovary and endometrium
 If occult blood stool is positive or if significant GI symptoms are present, a colonoscopy should
be done
 Pelvic sonograms are useful for smaller masses <8cm in premenopausal women
 Masses that are solid or multi-locular have a high probability of being neoplastic
 CA-125 should be measured
o Functional cysts
 An ovarian cyst is any collection of fluid surrounded by a very thin wall within an ovary.
o
o
o
 Any ovarian follicle >2cm = an ovarian cys
 Most are functional in nature and benign
 Occur most often during a woman's childbearing years
 Some ovarian cysts cause bleeding and pain
 Surgery may be required to remove cysts >5cm
Benign neoplasms
 Fibromas
 Most common benign ovarian neoplasm
 Occur most commonly in women of post-menopausal age
 Unilateral tumors, often at least 3cm in size
 Connective tissue tumors that arise from the ovarian cortical stroma
 If the stroma is estrogenic or luteinized, the tumors are thecomas
 Teratomas
 A tumor that consists of differentiated tissue from all 3 germ layers
 Benign teratomas (mature teratomas or dermoid cysts) are likely to contain more of
the recognizable organic structures such as thyroid, bronchial and CNS tissue
 Ectodermal structures such as hair, teeth and skin predominate
 In most instances, simple excision of the tumor is adequate therapy
 Epithelial cystic tumors
 One third of all ovarian tumors are the serous type and two thirds of these are benign
 Serous tumors are characterized by a proliferation of epithelium resembling that which
lines the fallopian tubes
 Most commonly seen in women in their 40’s and 50’s
 Benign lesions (e.g. mucinous cystadenoma) may be unilocular or multilocular, have a
smooth lining surface and contain thin, clear, yellow fluid
 Mucinous cysts
 Usually smooth-walled
 Generally multi-locular and the mucus-containing loculi appear blue through the tense
capsules
 Can grow quite large, measuring up to 30cm
 Patients often present with ovarian torsion
 Most common in the third to fifth decades of life
 Larger size assoc. with an increased risk of rupture  pseudomyxoma peritonei
Carcinomas
 Derived from coelemic epithelium
 Histologic subtypes: serous (55%), mucinous (20%), endometroid (15%) and clear cell (5%)
 Serous tumors resemble fallopian tube epithelium
 Mucinous tumors resemble endocervial epithelium
 Endometorid tumors resemble endometrial carcinomas and are associated with endometrial
carcinomas and endometriosis
 Clear cell carcinomas are uncommon
S/S:
 Frequently absent early on
 Symptoms persist for several months before being recognized and diagnosed
 Abdominal pain or discomfort, an abdominal mass, bloating, back pain, urinary urgency,
consipation, tiredness
o
o
 Pelvic pain, abnormal vaginal bleeding or involuntary weight loss
Risk factors
 BRCA1 and 2, HNPCC, age, nulliparity, family history, HRT, obesity
Impact of staging on management and followup
 For selected women with stage IA and IB disease, surgery alone is effective in treating the
disease and no additional therapy is recommended
 In almost all other cases, chemotherapy is recommended in conjunction with surgery
Gestational Trophoblastic Disease
 Hydatidiform mole
o Irregular or heavy PAINLESS vaginal bleeding during the first or early second trimester
o May expel “vesicles” from the vagina, have XS nausea and even hyperemesis gravidarum
o Auscultation of the uterus is typically remarkable for the absence of fetal heart sounds
o Bigger than expected uterus
 Choriocarcinoma
o Vaginal bleeding
o S/S of malignant disease:
 Hemoptysis, cough, dyspnea, headaches, dizzy spells, “blacking out”, rectal bleeding
o Uterine enlargement or abdominal enlargement because uterine rupture, liver or theca-lutein cyst
o Neurologic signs such as partial weakness or paralysis, dysphasia, aphasia, unreactive pupils
 Management and follow-up
o hCG titers that are high for early pregnancy
o US is diagnostic
o Suction evacuation followed by sharp curettage of the uterine cavity, regardless of the duration of
pregnancy
o Can give oxytocin help stimulate uterine contractions and reduce blood loss
o Serial hCG to make sure it decreases
o If hCG levels plateau or rise at any time, chemotherapy should be initiated (methotrexate or
actinomycin D)
Sexual Assault/Domestic Violence
 Patients at increased risk for sexual assault = the young, mentally and physically disabled, the elderly
 Medical and psychosocial management
o Provide acute medical care, including a thorough PE
o Transition to long-term care needed for psychological recovery from the extreme loss of control and
great fear of death
o Test for gonorrhea, chlamydia, HIV, HepB, syphilis
 Prophylaxis is suggested as preventive therapy
o Emergency contraception and tetanus toxoid
 Prevalence and incidence of violence against women, elder abuse, child abuse
o 2miL women/year, 500,000 for elderly abuse, child violence is “epidemic”
 Screening methods for domestic violence
o It is important to ask all women if they feel safe at home (do this when you are alone with the patient)
o Ask if the patient has ever been hit, kicked, hurt or threatened by their partner
 Resources for victims of domestic violence
o National Domestic Violence Hotline, RAINN (Rape, Abuse, Incest National Network) hotline, National
Child Abuse Hotline, Elder Abuse Hotline, Disabled Person Abuse Hotline