Sjögren syndrome

 Keratoconjunctivitis sicca
Exocrine  Dry mouth, salivary hypertrophy
features  Xerosis

 Raynaud phenomenon
 Cutaneous vasculitis
Extraglandular  Arthralgia/arthritis
features  Interstitial lung disease
 Non-Hodgkin lymphoma

 Objective signs of decreased lacrimation (eg, Schirmer test)

 Positive anti-Ro (SSA) &/or anti-La (SSB)
Diagnostic  Salivary gland biopsy with focal lymphocytic sialoadenitis
findings  Classification: primary if no associated CTD, secondary if comorbid
CTD (eg, SLE, RA, scleroderma)

CTD = connective tissue disease; RA = rheumatoid arthritis; SLE = systemic lupus

erythematosus; SSA/SSB = Sjögren syndrome (antibody) A/B.

Voice deepening is a common (and possibly irreversible) sign of frank virilization as excess
androgens (eg, testosterone >150 ng/dL, dehydroepiandrosterone sulfate [DHEAS] >700 µg/dL)
lengthen and thicken the vocal cords, thereby changing their acoustic frequency and changing the
voice. Other clinical features of virilization include male-pattern baldness (eg, temporal hair
loss), increased muscle bulk, and clitoromegaly.

Patients with virilization require evaluation for ovarian and adrenal sources of androgen
production with total testosterone, 17-hydroxyprogesterone, and DHEAS levels. This patient's
virilization and ovarian mass are most likely due to a Sertoli-Leydig cell tumor, a type of sex
cord–stromal tumor that secretes high testosterone levels.

depot medroxyprogesterone acetate (DMPA)

DMPA is an effective, injectable contraceptive that does not require daily administration. It is
safe for most women, particularly those who have contraindications to intrauterine devices
and/or estrogen-containing contraceptives. DMPA is given as an injection every 3 months. A
common side effect is light, irregular vaginal bleeding (eg, amenorrhea).

Because they are safe and have few contraindications, progestin-only contraceptive pills are
commonly used in women who are breastfeeding. However, they do not consistently inhibit
ovulation and have a high failure rate (eg, 6%) because of a short half-life that requires strict
adherence to a daily schedule (eg, >3 hr late requires backup contraception).

All patients with mixed incontinence generally require bladder training with lifestyle changes
(eg, weight loss, smoking cessation, decreased alcohol and caffeine intake) and pelvic floor
muscle exercises (eg, Kegels). Patients who have limited or incomplete symptom relief with
bladder training may benefit from pharmacotherapy or surgery, depending on predominant type:

 In patients with urgency-predominant incontinence, oral antimuscarinics and timed

voiding (eg, urinating on a fixed schedule, rather than based on a sense of urgency) are
used (Choice C).
 In patients with stress-predominant incontinence due to weakened pelvic floor muscles
(eg, cystocele), surgery with a midurethral sling is performed
Urodynamic testing involves measurement of bladder filling and emptying (ie, cystometry),
urine flow, and pressure (eg, urethral, leak point). This testing is typically reserved for patients
with complicated urinary incontinence (ie, those who do not respond to treatment) or who are
considering surgical intervention.
Emergency contraception
Timing after
Method Efficacy Contraindications
intercourse
 Wilson disease
Copper-containing  Active pelvic infection
0-120 hr >99%
intrauterine device  Severe uterine cavity distortion

 Breast cancer
Progestin-releasing  Active pelvic infection
0-120 hr >99%
intrauterine device  Severe uterine cavity distortion

 None
Ulipristal 0-120 hr 98%-99%
 None
Oral levonorgestrel 0-72 hr 92%-98%
 None
Oral contraceptives* 0-72 hr 75%-89%
*Combined estrogen/progestin oral contraceptive pills containing levonorgestrel or norgestrel.

This patient's clitoromegaly (eg, clitoris protruding from the clitoral hood) and large adnexal
mass are most likely due to a Sertoli-Leydig cell tumor, a testosterone-secreting sex cord–
stromal tumor. Sertoli and Leydig cells are normally found in the testes but can develop in the
ovaries and produce testosterone, particularly after malignant transformation and cell
proliferation. The testosterone excess results in the clinical features often associated with this
tumor, including:

 Rapid-onset virilization: Testosterone and dihydrotestosterone affect peripheral tissues,

resulting in clitoromegaly, as seen in this patient. Additional features may include male-
pattern (bitemporal) balding, voice deepening, and increased muscle mass.
 Signs of estrogen deficiency: Testosterone inhibits hypothalamic GnRH and pituitary
FSH/LH release, resulting in low estrogen. Therefore, patients may develop breast
atrophy, vulvovaginal atrophy, dyspareunia, and oligomenorrhea.

Sertoli-Leydig cells are typically diagnosed at an early cancer stage, and management includes
surgical removal. Those with metastatic disease may require additional chemotherapy.

Intimate partner violence (IPV) is any type of physical, psychological, or sexual harm
committed by a partner or spouse. It affects all genders, ages, races, and sexual orientations and
is highly prevalent, with a lifetime risk of approximately 1 in 3 for women and 1 in 4 for men.
IPV results in significant morbidity (eg, physical injury, mental health disorders) and mortality,
accounting for nearly 15% of all homicides.

IPV particularly affects women of childbearing age; however, it is underreported because

patients are often reluctant to disclose IPV for multiple reasons, including denial, shame, self-
blame, and fear of retribution. The United States Preventive Services Task Force (USPSTF)
recommends that screening be performed in all women of childbearing age and appropriate
patients be given referral for support services.

Screening commonly includes questions, both open ended (eg, "How safe do you feel in your
relationship?") and specific (eg, "Have you ever been hit, slapped, or kicked by your partner?"),
to improve disclosure rates. Patients who screen positive should be further assessed for
immediate safety and given additional resources (eg, local shelter referral) for long-term
planning.

In patients age ≥30, the preferred cervical cancer screening is a Pap test with human
papillomavirus cotesting, and it should be performed every 5 years. Alternately, a Pap test alone
should be performed every 3 years. This patient's Pap test was normal 2 years ago.

This patient's unifocal, firm, white vulvar plaque is concerning for vulvar squamous cell
cancer. A risk factor for vulvar cancer is lichen sclerosus, as seen in this patient's prior
symptoms that resolved with corticosteroid cream. Patients with chronic lichen sclerosus have
continued inflammation and hyperplasia of the vulvar epithelium that can result in malignant
transformation and development of a neoplastic lesion. This lesion typically develops over the
labia majora and can become pruritic, friable, and ulcerated.

In patients with lesions concerning for malignancy, the best next step in management is vulvar
biopsy, which distinguishes between benign (eg, lichen sclerosus) and neoplastic disease. In
those with neoplastic changes, biopsy further determines the depth of invasion and differentiates
between noninvasive (ie, vulvar intraepithelial neoplasia) or invasive (ie, vulvar cancer) disease.
Patients with noninvasive disease can be treated with either medical therapy (eg, imiquimod) or
laser ablative therapy (Choice B). Those with invasive disease require surgery (eg, wide local
excision ± lymph node dissection) and possible chemoradiation.

Elevated estrogen and testosterone with LH/FSH imbalance (eg, high LH, normal FSH) occurs
with polycystic ovary syndrome (PCOS), in which rapidly pulsating GnRH causes increased LH
production. LH stimulates ovarian theca cells to produce androgens that are subsequently
aromatized to estrogen in the periphery (ie, adipose tissue). Therefore, signs of
hyperandrogenism (eg, acne, hirsutism) are common.

This patient has benign-appearing endometrial cells on Pap testing. Pap test reporting varies
by age:
  In women age <45, endometrial cells are not reported on Pap test results because this is a
common, benign finding, particularly during the first 10 days of the menstrual cycle (as
in this patient).
 In women age ≥45, endometrial cells are reported because this finding is more
concerning for endometrial hyperplasia or cancer, particularly in patients who are
postmenopausal, symptomatic (ie, abnormal uterine bleeding), or at high risk (eg,
unopposed estrogen from obesity, chronic anovulation).

During fetal AIS development, the testes produce anti-Müllerian hormone (AMH) and
testosterone. AMH acts on Müllerian structures (ie, uterus, upper one-third of vagina) and
causes their regression. In contrast, testosterone has no activity on peripheral tissues, and male
external genitalia (eg, penis, prostate) do not develop, defaulting to female external genitalia (eg,
lower two-thirds of vagina). Therefore, these patients appear phenotypically female at birth.

Pubertal patients with AIS typically have primary amenorrhea (ie, no uterus and a blind
vaginal pouch) and some secondary sexual characteristic development. Although the testes
produce normal male pubertal-range testosterone levels, patients have no acne and minimal to
no axillary and pubic hair due to peripheral androgen resistance. However, the increased
testosterone is aromatized to estrogen and results in breast development and tall stature.

Vulvar lichen planus

 Women age 50-60
 Vulvar pain or pruritus
 Dyspareunia
 Erosive variant (most common):
o Erosive, glazed lesions with white border
Clinical features
o Vaginal involvement ± stenosis
o Associated oral ulcers
 Papulosquamous variant:
o Small pruritic papules with purple hue

Diagnosis Vulvar biopsy

Treatment High-potency topical corticosteroids

Vulvar lichen planus is a chronic inflammatory disorder that can present with multiple glazed,
erythematous vulvar erosions bordered by white striae (ie, Wickham striae). Patients often have
associated vaginal and oral lesions. Treatment is with topical corticosteroids.

Human papillomavirus
Disease associations  Cervical cancer
 Vulvar & vaginal cancers
 Anal cancer
 Penile cancer
 Oropharyngeal cancer
 Anogenital warts
  Recurrent respiratory papillomatosis

 All female and male patients* age 11-26

(but may be given to those age 9-45)
Vaccine indications
 Not indicated in pregnancy

*Including those with a history of genital warts, abnormal Pap cytology, or positive
human papillomavirus DNA test.

This patient has pelvic organ prolapse (POP), the herniation of the pelvic organs (eg, bladder,
uterus, rectum) into the vagina due to weakened pelvic floor muscles (ie, levator ani complex)
from chronic increased intraabdominal pressure. Risk factors include increasing parity, obesity,
and advancing age. Women with anterior vaginal wall prolapse (ie, cystocele), such as this
patient, can have pelvic pressure and urinary symptoms (eg, retention, stress urinary
incontinence). However, many patients with POP are asymptomatic and incidentally diagnosed
on routine examination.

Management of POP is based on symptoms or complications:

 Partial ovarian torsion, due to intermittent adnexal rotation around the

infundibulopelvic ligament containing the ovarian vessels, causes temporary ovarian
vessel occlusion and pelvic pain (from ovarian ischemia). Patients classically have
nausea, vomiting, and intermittent pain that self-resolves (ie, no symptoms between
episodes) as spontaneous adnexal untwisting allows blood flow to return. Therefore,
Doppler ultrasound may show normal ovarian arterial and venous blood flow.
 Partial ovarian torsion can progress to complete ovarian torsion. Although torsion is
less common in the pediatric population, an ovarian mass (as in this patient) increases
the risk for complete torsion because the increased adnexal size and density make
spontaneous untwisting less likely. Complete torsion, typically triggered by physical
activity (eg, walking), presents with severe, constant, unilateral pelvic pain due to
ongoing ovarian ischemia.

 Human papillomavirus (HPV) vaccination is recommended to prevent HPV-related

disease; it is typically administered to those age 11-26 but can be given from age 9 to 45.
Cervical cancer screening with Pap testing begins at age 21 in immunocompetent patients
regardless of age of onset of sexual activity.

Premenstrual syndrome and

premenstrual dysphoric disorder

Clinical o Symptoms occur during luteal phase
features o Physical: bloating, fatigue, headaches, hot flashes, breast tenderness
o Affective: anxiety, irritability, mood swings, decreased interest; more
 severe in premenstrual dysphoric disorder

o Symptom/menstrual diary
Evaluation
o Selective serotonin reuptake inhibitor
Treatment
Neonatal withdrawal bleeding
o In utero: maternal estrogen stimulates fetal endometrial
proliferation
Physiology o After delivery: withdrawal of maternal hormones →
endometrial sloughing in neonate

o Light vaginal bleeding in first 2 weeks of life

o ± Additional signs of maternal estrogen exposure:
o Physiologic leukorrhea
Clinical features
o Labial swelling
o Breast hypertrophy ± galactorrhea

o Clinical diagnosis
Diagnosis & o Reassurance for parents
management o Resolves on its own within days

This 5-day-old girl has mucoid vaginal discharge with streaks of blood, the classic
findings of neonatal withdrawal bleeding. This benign condition is the most common
cause of vaginal bleeding in neonates and is due to withdrawal of maternal hormones.

In utero, maternal estrogen crosses the placenta and stimulates fetal endometrial
proliferation. At birth, withdrawal of maternal progesterone and the absence of the
trophic effect of maternal estrogen cause endometrial sloughing and light vaginal
bleeding, as seen in this patient. Bleeding typically occurs within the first 2 weeks of life
and is self-limited (<5 days). Other physiologic effects resulting from exposure to
maternal estrogen in utero include leukorrhea (thin, white vaginal discharge), labial
swelling, breast hypertrophy, and galactorrhea.

Diagnosis is clinical, and no treatment is required. Management is observation and

education and reassurance for parents.

o Asymptomatic patients, such as this one with no complications (eg, no urinary

retention or hydronephrosis on ultrasound), do not require treatment and can be
managed with reassurance and observation only.
o In contrast, symptomatic patients (eg, pelvic pressure) or those with complications
could benefit from treatment. Pelvic floor muscle (ie, Kegel) exercises are
recommended in these patients. Nonsurgical treatment is with pessary placement,
which helps restore pelvic anatomy and reduces the severity of symptoms
 (Choice B). Surgical management (eg, anterior vaginal wall repair) can be
offered to patients whose condition does not improve or those who decline
nonsurgical treatment.

Granulosa cell tumor

o Sex cord–stromal tumor
o ↑ Estradiol
Pathogenesis
o ↑ Inhibin

o Complex ovarian mass

o Juvenile subtype
o Precocious puberty
o Adult subtype
Clinical features
o Breast tenderness
o Abnormal uterine bleeding
o Postmenopausal bleeding

o Call-Exner bodies (cells in rosette pattern)

Histopathology
o Endometrial biopsy (endometrial cancer)
Management o Surgery (tumor staging)

o Elevated serum 17-hydroxyprogesterone is characteristic of congenital adrenal

hyperplasia. Female patients classically have virilized genitalia (eg, clitoral
hypertrophy, labial fusion), which are not seen in this patient.

Pubertal gynecomastia
 Imbalance of estrogens & androgens during midpuberty
Etiology (Tanner stages 3-4)

 Small (<4 cm) firm, unilateral or bilateral, subareolar mass

Clinical  No pathologic features (eg, nipple discharge, axillary
features lymphadenopathy, systemic illness)

 Reassurance & observation

Management  Resolution within a year


o
 Choriocarcinoma
 Advanced maternal age
Risk factors  Prior complete hydatidiform mole

 Amenorrhea or abnormal uterine bleeding

 Pelvic pain/pressure
 Symptoms from metastases (lung, vagina)
Presentation
 Uterine mass
 Elevated β-hCG level

 Chemotherapy
Treatment
Pubertal gynecomastia is a benign, physiologic condition characterized by gradually enlarging,
glandular breast tissue in adolescent boys. It most commonly occurs in boys age 12-14 during
midpuberty (Tanner stage 3-4) due to transiently increased testicular production of estrogen
compared with testosterone and peripheral conversion of prohormones to estrogen. Patients
typically have a small (<4 cm), firm, unilateral or bilateral, subareolar mass that may be tender to
the touch.
Primary ovarian insufficiency
 Amenorrhea at age <40
 Hypoestrogenic symptoms (eg, hot flashes)
Clinical features  ↑ FSH
 ↓ Estrogen

 Idiopathic
 Turner syndrome (45,XO)
 Fragile X syndrome (FMR1 premutation)
 Autoimmune oophoritis
Major causes
 Anticancer drugs
 Pelvic radiation
 Galactosemia

 Estrogen therapy (with progestin if intact uterus)

Management
FMR1 = fragile X messenger ribonucleoprotein 1.

The treatment of lichen sclerosus is aimed at improving symptoms (eg, vulvar pain and pruritus)
and to possibly prevent further disease progression. The first-line treatment is with
superpotent topical corticosteroids (eg, clobetasol), which decreases the chronic inflammation
associated with lichen sclerosus. In addition, continued topical corticosteroid therapy may also
prevent disease progression to vulvar intraepithelial neoplasia or vulvar cancer. Patients may
also use topical emollients for daily symptom management.
Infectious genital ulcers
Painful Herpes simplex virus  Pustules, vesicles, or small ulcers on
erythematous base
  Tender lymphadenopathy
 Systemic symptoms common

 Larger, deep ulcers with gray/yellow

exudate
 Well-demarcated borders & soft,
Haemophilus ducreyi (chancroid) friable base
 Severe lymphadenopathy that may
suppurate

 Usually single ulcer (chancre)

 Indurated borders & hard,
Treponema pallidum (syphilis)
nonpurulent base

Painless  Initial small, shallow ulcers (often

Chlamydia trachomatis serovars missed)
L1-L3 (lymphogranuloma  Then painful & fluctuant adenitis
venereum) (buboes)

This patient's painful, vesicular lesions with associated tender lymphadenopathy are due to
genital herpes simplex virus (HSV) infection. Primary HSV outbreaks are often associated with
systemic symptoms (eg, fever, headache), more painful lesions that persist for a longer duration,
and concomitant urinary retention.

Without treatment, most immunocompetent patients with primary HSV have spontaneous
resolution of symptoms within a week. However, many patients will experience disease
recurrence, particularly during the first year after primary infection. Afterward, recurrence
becomes less frequent due to improved cell-mediated immunity. Antivirals (eg, acyclovir,
valacyclovir) are used to reduce symptom duration and frequency of recurrences but do not
eliminate recurrences.
In patients with no contraindications to estrogen, menopausal hormone therapy (MHT) is first-
line treatment.

 Patients with an intact uterus require estrogen-plus-progesterone MHT (eg, estrogen-

progestin pills), which decreases the risk of endometrial cancer associated with
unopposed estrogen (Choice B).
 In contrast, patients without a uterus (eg, prior hysterectomy) can receive estrogen-
only MHT (eg, transdermal estrogen patch), which is preferred in these patients because
estrogen-plus-progesterone MHT has a small increased risk of breast cancer with long-
term (>3-5 years) use.

In patients with contraindications to estrogen (eg, breast cancer, venous thromboembolism),

second-line treatment for vasomotor symptoms is paroxetine, a selective serotonin reuptake
inhibitor that is typically well tolerated. In patients who have no relief from paroxetine or who
cannot take paroxetine (eg, current tamoxifen use), clonidine or gabapentin may be used.
However, these medications can be associated with intolerable side effects, including
hypotension (clonidine) and headache/dizziness (gabapentin).
Endometrial hyperplasia/cancer
Risk factors Excess estrogen
  Obesity
 Chronic anovulation/PCOS
 Nulliparity
 Early menarche or late menopause
 Tamoxifen use

 Heavy, prolonged, intermenstrual &/or postmenopausal

Clinical
bleeding
features
 Endometrial biopsy (gold standard)
Evaluation  Pelvic ultrasound (postmenopausal women)

 Hyperplasia: progestin therapy or hysterectomy

Treatment  Cancer: hysterectomy

PCOS = polycystic ovary syndrome.

Without treatment, endometrial hyperplasia can progress to cancer. In patients (such as this
one) who may desire future fertility, initial management is with progestin therapy (eg,
progestin-releasing intrauterine device), which counteracts estrogen's effects by inhibiting
endometrial proliferation and promoting differentiation. Follow-up is with repeat endometrial
biopsy (eg, every 3 months). Patients with stable or improved disease continue progestin
therapy, whereas those with progression to cancer typically require hysterectomy
 Classi
c congenital adrenal hyperplasia (CAH), due to 21-hydroxylase deficiency, typically presents
during infancy as a salt-wasting adrenal crisis; girls also have ambiguous genitalia. Nonclassic
CAH typically presents in young women with slowly progressive (over years) hyperandrogenism
and abnormal uterine bleeding; true virilization is uncommon. Both types of CAH cause elevated
17-hydroxyprogesterone, rather than testosterone, levels.

Combination oral contraceptive pills (OCPs) can be used in patients with symptomatic uterine
fibroids to decrease heavy menstrual bleeding. However, OCPs are less preferred in those
desiring future fertility because they do not decrease the risk of fibroid-related pregnancy
complications. In addition, this patient's migraine with aura is a contraindication to OCPs due to
increased stroke risk.

This patient with pelvic pain, bloating, and a decreased appetite has a complex adnexal mass
(ie, solid components and thick septations) with ascites on imaging, which is worrisome for
advanced-stage epithelial ovarian carcinoma (EOC).

The ovary is composed of multiple different cell lineages, each of which can result in different
malignancies (eg, granulosa cell tumors arise from stromal cells, yolk sac tumors arise from
germ cells). EOC is the most common subtype of ovarian cancer and is thought to arise from the
ovarian surface epithelium.

Recent studies have revealed that the majority of EOC tumors are most histologically and
molecularly similar to fallopian tube epithelium. For most cases, epithelial ovarian
carcinogenesis is thought to originate from the dysplastic/malignant tubal epithelium that
spills secondarily onto the surface of the ovary (creating the appearance of ovarian origin), the
peritoneum, and the omentum. Salpingectomies remove the entire tube (not just a portion) and
markedly reduce the risk of EOC (up to 40% risk reduction). For other cases of EOC, the
ovarian surface epithelium is thought to undergo malignant transformation after sustained
damage with persistent ovulation, which is why suppression of ovulation (ie, oral contraceptive
pills, pregnancy) protects against the development of EOC.

Patients with long-term intrauterine devices (IUDs) are at increased risk for Actinomyces
infection because this bacterium can ascend to the upper genital tract to colonize an indwelling
IUD. However, there is not a strong association between IUD use and recurrent vulvovaginal
candidiasis;
Interstitial cystitis (bladder pain syndrome)
 More common in women
Epidemiology  Associated with psychiatric & pain disorders (eg, fibromyalgia)

 Bladder pain with filling, relief with voiding

 ↑ Urinary frequency, urgency
Clinical presentation
 Dyspareunia

 Bladder pain with no other cause for ≥6 weeks

Diagnosis  Normal urinalysis

 Not curative; focus is on improving quality of life

 Behavioral modification, avoidance of triggers, physical therapy
Treatment  Amitriptyline, pentosan polysulfate sodium
 Analgesics for acute exacerbations

Other clinical features include urinary frequency and urgency, chronic pelvic pain, and
dyspareunia. IC typically presents in women age >40 and is associated with other chronic pain
conditions (eg, fibromyalgia, endometriosis, irritable bowel syndrome), sexual dysfunction, and
psychiatric illness (eg, depression, anxiety).

A urethral diverticulum, an abnormal outpouching of the urethra, can cause urethral tenderness,
urinary frequency, and dyspareunia. However, it also typically presents with a tender anterior
vaginal mass, purulent urethral discharge, and increased pain with voiding.
Intraductal papilloma
 Benign papillary tumor arising from breast duct lining
Pathology
 Unilateral, bloody nipple discharge (can be nonbloody)
Clinical features  No associated breast mass or lymphadenopathy

 Mammography & ultrasonography

Management  Biopsy ± excision
The most common (~50%) cause of unilateral bloody nipple discharge without a coexisting
breast mass or lymphadenopathy is a benign intraductal papilloma. Intraductal papillomas
are papillary projections composed of epithelial and myoepithelial cells. These cells line a
fibrovascular stalk that protrudes into the breast duct lumen; twisting of the stalk causes
intraluminal bleeding and subsequent bloody nipple discharge.

On examination, intraductal papillomas are typically nonpalpable due to small size (≤1 cm) and
intraductal location. Although most cases of pathologic nipple discharge are caused by benign
intraductal papillomas, some breast cancers can also present with associated nipple discharge;
therefore, all patients with pathologic nipple discharge require further evaluation with breast
imaging.

Certain antipsychotic medications (eg, risperidone) induce dopamine blockade in the pituitary.
Because dopamine normally inhibits prolactin secretion, use of these antipsychotics can lead to
hyperprolactinemia and subsequent galactorrhea.
 Hyperandrogenism
Clinical features  Hirsutism
  Nodulocystic acne
 Androgenic alopecia
 ↑ Serum testosterone

 Polycystic ovary syndrome

 Androgen-secreting tumor
Differential diagnosis  Cushing syndrome
 Nonclassical CAH

CAH = congenital adrenal hyperplasia.

A Gartner duct cyst results from incomplete regression of the Wolffian duct during fetal
development. These cysts appear along the lateral aspects of the upper anterior vagina.

Skene glands are bilateral paraurethral glands in the anterior vaginal vestibule. Skene gland cysts
may form with duct obstruction but would be located lateral to the urethral meatus.

Trastuzumab is a monoclonal antibody often used in combination with adjuvant chemotherapy

in patients with human epidermal growth receptor 2 (HER2)-positive breast carcinoma.
Cardiotoxicity is a known adverse effect of trastuzumab that usually manifests as an
asymptomatic decline in left ventricular ejection fraction; however, overt heart failure can occur.
The risk and extent of cardiotoxicity are amplified when trastuzumab is used in combination with
chemotherapy agents that are also cardiotoxic (eg, doxorubicin).
Prior to initiating trastuzumab, patients should undergo a baseline assessment of cardiac
function by echocardiography. In addition, cardiac function should be reassessed by
echocardiography at regular intervals during therapy. Therapy should be discontinued in patients
who develop symptomatic heart failure or a significant decline in ejection fraction (eg, >16
percentage points from baseline). The cardiotoxicity associated with trastuzumab is typically
reversible, with patients experiencing complete recovery of cardiac function following treatment
discontinuation.
Clinical suspicion is critical to diagnosis because of CVT's astonishingly variable presentation,
stemming largely from cerebral venous anatomy that crosses arterial territories (ie, broad range
of neurologic dysfunction). Cerebral venous sinuses' unique anatomic function of cerebrospinal
fluid (CSF) drainage, in addition to blood return from cerebral veins, results in 2
pathophysiologic mechanisms of thrombosis:

 Venous sinus obstruction impairs CSF absorption, causing increased intracranial

pressure (eg, headache, papilledema).
 Venous sinus and isolated cerebral vein obstruction impedes blood return, causing
increased venule/capillary pressure, resulting in decreased cerebral perfusion (cytotoxic
edema) and blood-brain barrier disruption (vasogenic edema). This produces focal
deficits that correspond to venous drainage territories (eg, sagittal sinus or cortical vein
thrombosis obstructs cortical blood return, producing motor deficits and seizures).
Magnesium sulfate treats eclampsia, which can occur up to 6 weeks postpartum and presents
with seizures and headache. This patient's normal blood pressure and lack of proteinuria make
this diagnosis less likely.

Placenta accreta
 Morbidly adherent placental attachment to the myometrium
Definition
 Placenta previa + prior uterine surgery (eg, cesarean delivery, D&C,
Risk factors myomectomy)

 Prenatal diagnosis: US with placenta previa, numerous placental

Clinical lacunae, myometrial thinning
features  Postpartum diagnosis: adherent placenta, postpartum hemorrhage

 Cesarean hysterectomy with placenta in situ

Management
D&C = dilation & curettage; US = ultrasound.
Uterine inversion can cause postpartum hemorrhage as the result of excessive traction on the
umbilical cord and an abnormally adherent placenta. However, patients typically have severe
abdominal pain and a smooth mass protruding from the cervix or vagina.

The tetanus-diphtheria-pertussis (Tdap) vaccine protects against pertussis, which has high infant
morbidity and mortality. Maternal vaccination occurs at 27-36 weeks gestation to maximize
transplacental antibody transfer for fetal protection. Early (eg, initial prenatal visit) or late
maternal vaccination results in suboptimal fetal protection.

Nausea and vomiting are common during pregnancy. In women with mild nausea and vomiting
(as in this patient with nausea without vomiting), changes in vital signs, or weight loss, the initial
approach is conservative treatment with dietary changes or vitamin B6 (pyridoxine) prior to
prescribing antiemetic medications.