REPRODUCTIVE SYSTEM (7%) Flashcards

Question 1

Q

OVARIAN TORSION

Answer

A

Ovarian torsion refers to the rotation of the ovary at its pedicle to such a degree as to occlude the ovarian artery and/or vein

complete or partial rotation of ovary on its ligamentous supports

⦁ ovary typically rotates around both the infundibulopelvic ligament (connects ovary to fallopian tube) + utero-ovarian ligament (connects ovary to uterus)

Ovarian torsion (OT) is when an ovary twists on its attachment to other structures, such that blood flow is decreased

Patients with ovarian torsion often present with sudden onset of sharp and usually unilateral lower abdominal pain

70% of cases accompanied by nausea and vomiting

Complications may include infection, bleeding, or infertility

this often results in loss of blood supply
the fallopian tube often twists along with the ovary = adnexal torsion

Ovarian torsion = rare event

reported with both normal + pathologic fallopian tubes
50-60% = SECONDARY TO OVARIAN MASS
MC cause = ovarian cyst
Ovarian torsion usually occurs in ovarian masses measuring > 5 cm in diameter.
RIGHT ovarian torsion = MORE COMMON than left (perhaps because right utero-ovarian ligament is longer than the left, or that presence of sigmoid colon on left side helps prevent it

SIGNS / SYMPTOMS
⦁ abrupt onset of acute, severe, unilateral, lower abdominal + pelvic pain with guarding
⦁ pain is ** NON-RADIATING **
⦁ often associated with N/V
⦁ often the severe pain comes on suddenly with a change in position
⦁ a unilateral, extremely tender adnexal mass is found in > 90% of patients
⦁ many patients noted intermittent previous episodes of similar pain for several days to several weeks

PELVIC EXAM
= adnexal tenderness
- no cervical motion tenderness
- no change in discharge
- no urinary discomfort
- no bleeding (ectopic)

** often confused with appendicitis **

** severe acute unilateral lower abdominal or pelvic pain with N/V
brought on by changing positions
tender adnexal mass
Patients with ovarian torsion often present with sudden onset of sharp and usually unilateral lower abdominal pain

70% of cases accompanied by nausea and vomiting

do NOT cause shock (fever / hypotension / tachycardia)

DIAGNOSIS
⦁ color flow Doppler US - transvaginal - presence of spikes = IMAGING OF CHOICE

Transvaginal doppler ultrasound is the diagnostic test of choice and will show no flow in the ovary*****
- but doppler flow is not always absent with ovarian torsion

A negative pregnancy test in conjunction with the presence of spikes along the doppler flow graph is diagnostic for ovarian torsion.

⦁ CT with contrast ( to also rule out other causes)

⦁ GOLD STANDARD for diagnosis = LAPAROSCOPY

TREATMENT
⦁ early diagnosis can often be managed with conservative laparoscopic surgery to uncoil twisted ovary

⦁ may perform oophoropexy to fixate the ovary which is likely to twist again

⦁ if necrosis is developing = need unilateral salpingo-oophorectomy = TOC

salpingo-oophorectomy = surgery to remove the ovaries and fallopian tubes. Removal of one ovary and fallopian tube is called a unilateral salpingo-oophorectomy. When both are removed, it’s called a bilateral salpingo-oophorectomy

Question 2

Q

TRICHOMONIASIS

Answer

A

Trichomoniasis is a common cause of vaginitis.

most common non-viral STD worldwide

It is a common sexually transmitted infection, and is caused by the single-celled protozoan PARASITE** - Trichomonas vaginalis

⦁ Bacteria = Trichomonas vaginalis (T. vaginalis)
⦁ PEAR shaped FLAGELLATED PROTOZOA
⦁ sexually transmitted

Men = typically asymptomatic

Produces mechanical stress on host cells and then ingesting cell fragments after cell death.

Trichomoniasis is primarily an infection of the UROGENITAL TRACT

MC site of infection = urethra and vagina in women

Trichomonas vaginalis is transmitted through sexual contact, as it cannot exist outside the body.

SYMPTOMS
⦁	vulvar pruritus
⦁	vulvovaginal erythema
⦁	itching
⦁	burning
⦁	dysuria
⦁	dyspareunia
⦁	post-coital bleeding

⦁ MALODOROUS VAGINAL DISCHARGE

copious, malodorous discharge
FROTHY YELLOW-GREEN DISCHARGE - THICK / FOUL ODOR
discharge is worse with menses

⦁ STRAWBERRY CERVIX (cervical petechiae)
= erythematous cervix + pinpoint areas of exudation

: A relatively small proportion of women with trichomonas vaginalis will have ‘“strawberry cervix”. It is so named because of the erythematous appearance and pinpoint areas of exudation - strawberry-like.

Vaginal pH > 5
(normal vaginal pH = 3.8 - 4.5)

DIAGNOSIS
⦁	wet mount = motile protozoa (trichomonads) = "CORKSCREW" motility - FLAGELLA ****
⦁	elevated WBC count
⦁	vaginal pH 5-6
⦁	UA = positive for WBCs

** MOBILE WET PREP **

⦁ Nucleic acid amplification test = gold standard for the diagnosis of T. vaginalis, but is used only in women with non-diagnostic or negative wet mount.

For women with non-diagnostic (or negative) wet-mount slides on microscopy, nucleic acid amplification tests (NAAT) are performed

TREATMENT
⦁ Metronidazole (Flagyl)
- either 2g oral x 1 dose (500mg x 4 pills at once) or 500mg bid oral x 7 days

safe to use in pregnancy!

⦁ Tinidazole

** MUST ALSO TREAT PARTNER **

COMPLICATIONS

perinatal complications
increased HIV transmission

Patient will present as → a 27-year-old female complaining of a malodorous vaginal discharge. Her past medical history is unremarkable, and she does not take any medications. She is sexually active with one male partner and uses condoms inconsistently. Pelvic examination is notable for a yellow-green, malodorous discharge. Vaginal pH is 5.6. Urinalysis is positive for white blood cells. Saline microscopy demonstrates motile trichomonads. She is started on metronidazole and she is told that her partner must be started on the same medication.

Question 3

Q

BACTERIAL VAGINOSIS (BV)

Answer

A

Bacterial vaginosis (BV), also known as vaginal bacteriosis or Gardnerella vaginitis, is a disease of the vagina caused by excessive growth of bacteria.

CAUSE
⦁ Gardnerella vaginalis = a pleomorphic, gram-variable rod (anaerobic) involved in bacterial vaginosis.

Decreased Lactobacilli acidophilus (maintains normal vaginal pH) –> causes the overgrowth of NORMAL FLORA (GARDNERELLA VAGINALIS), and other anaerobes
a result of disruption in the normal vaginal microflora

BV = MC CAUSE OF VAGINITIS

BV is not an STD that can be passed on, but it is associated with sexual activity

SYMPTOMS
Common symptoms include 
⦁	increased vaginal discharge - white or grey 
⦁	fishy odor
⦁	vaginal odor worse after sex
⦁	may have dysuria (burning with urination)
⦁	may be asymptomatic
⦁	may have pruritus, not as common

FISHY, grey, scant, THIN, STICKY discharge

BV increases the risk of infection by a number of other sexually transmitted infections including HIV/AIDS
It also increases the risk of early delivery among pregnant women
Bacterial vaginosis is associated with sexual activity however it is not considered to be sexually transmitted

DIAGNOSIS
⦁ KOH test - release of amine odor (+ whiff test)
⦁ Wet prep or wet mount (saline) = “ CLUE CELLS “
- squamous epithelial cells of vagina with a STIPPLED appearance from being covered with bacteria
⦁ vaginal pH > 4.5 (normal = 3.8-4.2)
⦁ Few WBCs (unlike trich / PID)
⦁ Few lactobacilli

The diagnosis of bacterial vaginosis is made when 3/4 Amsel criteria are met.
- The Amsel criteria are as follows:
⦁ 1) Thin, gray-white or yellow vaginal homogenous discharge
⦁ 2) Clue cells (vaginal epithelial cells with adherent bacteria) on microscopy
⦁ 3) Vaginal fluid pH > 4.5
⦁ 4) A fishy odor upon addition of alkali (ie. KOH)

TREATMENT
⦁ 1st = Metronidazole (Flagyl) - 500mg bid x 7 days
- safe in pregnancy
- may also use gel (not as effective)

⦁ Clindamycin
- gel or PO

PREVENTION
⦁ avoid douching - promotes loss of lactobacilli

TREATING PARTNER IS UNNECESSARY
- unclear if BV is sexually transmitted, but reduced recurrence if condoms are used

COMPLICATIONS
⦁ premature rupture of membranes (PROM)
⦁ preterm labor
⦁ chorioamnionitis

Question 4

Q

PELVIC INFLAMMATORY DISEASE (PID)

Answer

A

PID = infection of the upper part of the female reproductive system = the uterus, fallopian tubes, and ovaries, and inside of the pelvis.

** MC CAUSE = CHLAMYDIA ***
next mc = gonorrhea

RISK FACTORS
⦁	hx of new or multiple sexual partners
⦁	unprotected sex
⦁	prior PID or STIs
⦁	age 15-19, or age < 25
⦁	nulliparous
⦁	IUD

SYMPTOMS
⦁	lower abdominal pain / *guarding*
⦁	** cervical motion tenderness ** = "chandelier sign"
⦁	mucopurulent vaginal discharge
⦁	fever
⦁	dysuria (burning with urination)
⦁	dyspareunia
⦁	irregular menstruation
- may be asymptomatic

CLASSIC TRIAD =

1) Pelvic pain
2) increased vaginal discharge
3) fever

COMPLICATIONS (if left untreated)
⦁	infertility
⦁	ectopic pregnancy
⦁	sepsis
⦁	chronic pelvic pain
⦁	tubo-ovarian abscess
⦁	hydrosalpinx (blocked fallopian tube filled with clear or serous fluid)
⦁	cancer

DIAGNOSIS
⦁	clinical
⦁	ultrasound
⦁	WBC count > 10,000
⦁	positive GC or chlamydia

Tubal wall edema, visible hyperemia of the tubal surface, and the presence of exudate on the tubal surfaces and fimbriae are the minimum criteria for laparoscopic diagnosis of pelvic inflammatory disease.

Actinomycosis can be characterized by the formation of multiple abscesses and sinus tracts containing sulfur granules. It is an uncommon cause of pelvic infection, but is associated with an indwelling IUD
= Gram-positive filamentous rods
= TX = IV PCN G

TREATMENT
o Outpatient
⦁	Ceftriaxone + Doxycycline 100mg BID x 14 days
(if PID = want doxycycline)
- with or without metronidazole

Doxycycline = MC used oral antibiotic in the treatment of PID

or
⦁ Ceftriaxone + Azithromycin

o Inpatient
⦁ IV Doxycycline + Cefoxitin or Cefotetan (2nd gen)
- or Clindamycin + Gentamycin (used for endometritis)

Fitz-Hugh-Curtis syndrome: perihepatitis + PID

Fitz-Hugh-Curtis syndrome is a rare complication of PID involving inflammation of the liver capsule and formation of ‘violin string’ adhesions.

This leads to right upper quadrant pain and/or tenderness, occasionally with radiation to the right shoulder

don’t have elevated liver enzymes, as liver is not inflamed, only liver capsule is
Chlamydia = MC cause of fitz-hugh-curtis syndrome
Hepatic fibrosis / scarring + peritoneal involvement
RUQ pain due to perihepatitis (liver capsule)
may radiate to right shoulder
normal LFTs
“violin string” adhesions on anterior liver surface
complications = infertility, TOA, ectopic pregnancy, chronic pelvic pain

Patient will present as → a 27-year-old female who comes to the emergency department with a 2-day history of lower abdominal pain, fever, chills, and malaise. The patient also complains of nausea and multiple episodes of vomiting in the past 24 hours. On physical examination, there is bilateral adnexal tenderness, mucopurulent cervical discharge, and cervical motion tenderness.

Question 5

Q

TUBO-OVARIAN ABSCESS (TOA)

Answer

A

Tubo-ovarian abscesses are inflammatory masses found in the ovary or fallopian tube and may extend to adjacent structures

TOA = an inflammatory mass involving the fallopian tube, ovary, and, occasionally, other adjacent pelvic organs (eg, bowel, bladder)

TOA typically occurs as a complication of PID.
These abscesses are found most commonly in reproductive-age women and typically result from upper genital tract infection

TOA may occur without preceding PID

Tubo-ovarian abscess (TOA) is an inflammatory mass found in the fallopian tube, ovary and adjacent pelvic organs. TOAs occur in about 15% of women with pelvic inflammatory disease (PID)

TOA is a serious and potentially life-threatening condition. Aggressive medical and/or surgical therapy is required, and rupture of an abscess may result in sepsis

CAUSES
A tubo-ovarian abscess usually presents in young women with an upper genital tract infection as a severe complication of PID or from local spread of an inflammatory disease of the bowel or adnexal surgery.

They tend to be polymicrobial infections with both aerobic and anaerobic bacteria.

The most common organisms include 
⦁	Escherichia coli
⦁	Streptococci
⦁	Bacteroides fragilis
⦁	Prevotella. 
⦁	Intrauterine devices are associated with Actinomyces israelli

** Interestingly, both N. gonorrhea and C. trachomatis are rarely isolated from a TOA ** (even though they are the MC organisms in PID)

The major risk factors for TOA are:

1) Multiple sexual partners
2) Prior history of PID
3) Age 15-40 years old (reproductive age women)
4) abdominal/pelvic surgery (ex: hysterectomy)

SYMPTOMS
They are characterized by 
⦁	acute lower abdominal pain
⦁	fever
⦁	chills
⦁	dyspareunia
⦁	vaginal discharge
⦁	N / V
⦁	+/- abnormal vaginal bleeding

PID can present in a similar manner

Mucopurulent (green or yellow) discharge on speculum examination and acute cervical motion tenderness, uterine or adnexal tenderness are indicative for PID and TOA

Pain that is severe, intermittent and unilateral with associated nausea and vomiting is more consistent with a TOA
Women with a ruptured TOA can present with signs and symptoms of an acute abdomen and sepsis.

DIAGNOSIS
⦁ Ultrasound = best initial test
- would show complex multilocular masses that disrupt the normal architecture of the ovary/ fallopian tube, + internal echoes consistent with inflammatory debris
⦁ UA
⦁ blood work - elevated WBC count + left shift
⦁ vaginal + blood cultures
⦁ CT
- An abdominal/pelvic CT scan is preferred if a GI tract process is strongly considered in the differential.

When a patient presents with classic signs and symptoms of a TOA and is hemodynamically stable, then a TVUS or pelvic CT should be ordered.

However, if the study is non-diagnostic or if the patient is unstable (indicative of a potential ruptured TOA), then a diagnostic laparoscopy or laparotomy should be performed, and the Gynecology service consulted to evaluate the patient. Moreover, if a postmenopausal women presents with evidence for a TOA, then surgical evaluation is indicated because of the higher incidence of associated malignancy.

TREATMENT
⦁ The large majority of small abscesses (<7 cm in diameter) resolves with antibiotic therapy alone

broad spectrum antibiotics if the patient is stable and the abscess is less than 9 cm

All patients with a high suspicion for a TOA need to be hospitalized and IV antibiotics immediately started.

treatment modalities include: antibiotic therapy, minimally invasive drainage procedures, invasive surgery, or a combination of these interventions

⦁ Cefoxitin (2 grams IV q6h) or cefotetan (2 grams IV q12h) and doxycycline (100 mg orally or IV q12h)

⦁ Ampicillin (2 grams IV q6h) + gentamicin (2 mg/kg IV loading dose, then 1.5 mg/kg IV q8h) +clindamycin (900 mg IV q8h)

⦁ Ampicillin/sulbactam (3 grams IV q6h) and doxycyline 100 mg IV or oral q12h)

Antibiotic therapy alone is usually effective in about 70% of patients. However, if the patient does not meet these criteria or has any evidence of a ruptured TOA, then surgery is indicated – either a laparoscopy or laparotomy. Surgery involves the removal of the abscess cavity and irrigation of the peritoneal cavity with both aerobic and anaerobic cultures sent.

Question 6

Q

OVARIAN CYST

Answer

A

An ovarian cyst = any fluid-filled sac within the ovary

Ovarian cyst = sac filled with liquid or semi-liquid material in an ovary

the vast majority of ovarian cysts are benign

Most women of reproductive age develop small cysts each month

Large cysts that cause problems occur in about 8% of women before menopause

Ovarian cysts are present in about 16% of women after menopause = are more likely to be cancer

SYMPTOMS
⦁ most are ASYMPTOMATIC until they rupture, undergo torsion, or become hemorrhagic

Occasionally they may produce
⦁ bloating
⦁ dull-aching lower abdominal pain or
⦁ lower back pain (may radiate from abdomen to back)

If the cyst either ruptures or gets torsed ==> severe sharp pain may occur
⦁ sharp unilateral RLQ or LLQ pain
⦁ vomiting
⦁ feeling faint
⦁ menstrual changes (abnormal uterine bleeding)
⦁ dyspareunia

PHYSICAL EXAM
⦁ unilateral pelvic pain / tenderness
⦁ may have mobile palpable cystic adnexal mass

Dyspareunia is associated with ovarian cysts due to endometriosis.

The majority of cysts are, however, harmless

CAUSES OF OVARIAN CYSTS
⦁ hormonal imbalances
⦁ carcinomas
⦁ normal physiologic functions of the ovary

There are two types of cysts: Functional and Nonfunctional

o FUNCTIONAL CYSTS = form as a normal part of the menstrual cycle

⦁ Follicular cyst = MC type of ovarian cyst

In menstruating women, a follicle containing the ovum (unfertilized egg) will rupture DURING OVULATION
If not , a follicular cyst > 2.5cm may result
most resolve within 6-8 weeks (2 menstrual cycles)
If the pt makes a lot of follicular cysts you may consider placing them on OCPs
If > 6 cm there is a risk of torsion and generally don’t self-resolve. Could consider surgical removal.

⦁ Corpus luteum cysts appear AFTER OVULATION when corpus luteum fails to degenerate.

The corpus luteum is the remnant of the follicle after the ovum has moved to the fallopian tubes
This normally degrades within 5–9 days. A corpus luteum that is more than 3 cm is defined as cystic.
Average size 4cm
Can have bleeding within the cyst and can rupture
Pain immediately after sex is a common presentation
Often occur on the right side due to increased luminal pressure from the Inferior Vena Cava
Rupture usually occurs day 16-20 of the menstrual cycle
Menses may be delayed days to weeks with subsequent menorrhagia (heavy menses)

Corpus luteum cysts tend to be larger and more symptomatic than follicular cysts and are more prone to hemorrhage and rupture. Follicular cysts are usually smaller, with internal hemorrhage being relatively uncommon.

⦁ Theca lutein cysts occur due to excessive B-hCG, which causes hyperplasia of theca interna cells- these cysts usually develop on BOTH OVARIES.

o NON-FUNCTIONAL CYSTS = not a normal part of menstrual cycle
⦁ PCOS
- Lack of regular menses with chronic anovulation
- Obesity, hirsutism, acne, amenorrhea or oligomenorrhea, menarche occurs at an expected age. - Strongly associated with obesity, acanthosis nigricans, insulin resistance, and hyperinsulinemia

⦁	Chocolate Cysts (caused by endometriosis)
⦁	Hemorrhagic ovarian cyst
⦁	Dermoid cyst: Teratoma
⦁	Ovarian serous cystadenoma
⦁	Ovarian mucinous cystadenoma
⦁	Paraovarian cyst
⦁	Cystic adenofibroma
⦁	Borderline tumoral cysts

Dermoid Cyst = benign cystic tumors composed of mature cells. Benign teratomas such as dermoid tumors are among the most common ovarian neoplasms, but not most common type of ovarian cyst

Some common cyst types are corpus luteum cysts, theca-lutein cysts, dermoid cysts, endometroid cysts etc.

o Corpus luteum cyst = an ovarian cyst that forms due to hemorrhage into a persistent corpus luteum

o Theca-lutein cysts often occur as multiple ovarian cysts due to gonadotropin stimulation and are associated with choriocarcinoma and moles

o Dermoid cyst = an ovarian cyst that is described as a mature teratoma

o Endometrioid cyst (chocolate cyst) = an ovarian cyst that forms due to endometriosis

o Hemorrhagic cyst = an ovarian cyst that is due to blood vessel rupture in the cyst wall and one that grows with increased blood retention.

DIAGNOSIS
⦁ Ultrasound = best initial test
⦁ pregnancy test
⦁ ** GOLD STANDARD = LAPAROSCOPY **

Ultrasonography is the preferred imaging modality for assessing gynecologic structures, given its low cost, availability, and sensitivity in recognizing adnexal cysts and hemoperitoneum. Despite this, ultrasound findings are nonspecific in some instances, particularly after rupture and decompression of a cyst in the setting of apparent physiologic levels of fluid in the pelvis. If ultrasound yields ambiguous results in a patient with significant pain, CT of the pelvis with contrast should be performed.

1) Follow-up imaging in women of reproductive age for incidentally discovered simple cysts on ultrasound is not needed until 5 cm, as these are usually normal ovarian follicles
2) For simple cysts >/= 5 cm but < 7 cm in premenopausal females, cysts should be followed yearly
3) For simple cysts >/= 7 cm, further imaging with MRI or surgical assessment is mandated as these cysts cannot be reliably assessed by ultrasound alone
4) Elevated CA-125, a tumor marker, is often found in increased levels in ovarian cancer

TREATMENT
o Mainstay of TX for majority of ovarian cysts = OBSERVATION

About 95% of ovarian cysts are benign

⦁ Ovarian cysts < 5 cm don’t usually require long-term follow up. If ovarian cysts are 5cm + = require f/u imaging. if ovarian cysts are 7cm+ = require MRI f/u

most cysts < 8cm are functional, and usually spontaneously resolve
⦁ rest
⦁ NSAIDS
⦁ repeat US in 6 weeks***
⦁ OCPs = may prevent recurrence, but doesn’t treat existing cysts
If > 8cm or if persistent or if cysts are postmenopausal ==> LAPAROSCOPY / LAPAROTOMY

Functional cysts (follicular / corpus luteum / theca lutein) and hemorrhagic ovarian cysts usually resolve spontaneously. However the bigger an ovarian cyst is, the less likely it is to disappear on its own

Treatment may be required if cysts persist over several months, grow, or cause increasing pain

⦁ The management of SYMPTOMATIC ovarian cysts
> 5cm = laparoscopic surgical removal

Cysts that persist beyond 2-3 menstrual cycles, or occur in postmenopausal women, should be investigated through ultrasonography and laparoscopy, especially in cases where family members have had ovarian cancer. Such cysts may require surgical biopsy

Patient will present as → a 22-year-old nulligravida presents with pelvic pain and irregular menstrual bleeding. She denies sexual activity, and her β-hCG urine test is negative. She has never been on oral contraceptives. On pelvic examination, unilateral tenderness on the left side and a palpable cystic mass approximately 4 to 5 cm in size is present.

Question 7

Q

RUPTURED OVARIAN CYST

Answer

A

Ruptured ovarian cysts are common and can be either asymptomatic or associated with unilateral lower abdominal pain during physical activity (exercise, sexual intercourse).

SYMPTOMS
Cyst rupture is characterized by
⦁ sudden, unilateral, sharp pelvic pain
⦁ can be associated with trauma, exercise, or coitus

In addition, cyst rupture can lead to
⦁ peritoneal signs
⦁ abdominal distention
⦁ bleeding that is usually self-limited

do NOT cause shock (fever / hypotension / tachycardia)

DIAGNOSIS
⦁ Ultrasound
- would show an ovarian cyst and the presence of blood or serous fluid in the pelvis

Fluid is anechoic on ultrasound

Ultrasonography = preferred imaging modality for assessing gynecologic structures, given its low cost, availability, and sensitivity in recognizing adnexal cysts and hemoperitoneum

Despite this, ultrasound findings are nonspecific in some instances, particularly after rupture and decompression of a cyst in the setting of apparent physiologic levels of fluid in the pelvis
If ultrasound yields ambiguous results in a patient with significant pain, pelvic CT with contrast should be performed.

Question 8

Q

CA-125 TESTING

Answer

A

cancer antigen 125 (CA-125) testing is often used to investigate for ovarian cancer.

contraindications to CA-125 testing
⦁	Pregnancy
⦁	ovarian cyst accidents
⦁	peritonitis
⦁	hemorrhage
⦁	cyst rupture
⦁	infection
⦁	menstruation
⦁	fibroids
⦁	endometriosis

CA-125 testing should not be done in pregnant patients with ovarian cysts because levels are significantly higher, especially during the first trimester. CA-125 testing should also not be done in the acute setting of ovarian cyst accidents, as this marker is raised in peritonitis, hemorrhage, cyst rupture, and infection, as well as in menstruation, fibroids, and endometriosis.

The reference range of CA 125 is 0-35 units/mL
if 35+ units / mL = requires further treatment

Question 9

Q

PCOS = POLYCYSTIC OVARIAN SYNDROME

Answer

A

PCOS = presence of ovarian cysts, however, ovarian cysts are no longer a required characteristic of PCOS

PCOS = dysfunction in the hypothalamic-pituitary- ovarian axis

2 PHASES OF MENSTRUAL CYCLE
⦁ Follicular phase = before ovulation (first 14 days)
⦁ Luteal phase = after ovulation

FOLLICULAR PHASE

hypothalamus releases GnRH
GnRH acts on anterior pituitary gland–> release gonadotropins (FSH / LH) - released in pulses
FSH + LH travel to follicles in the ovaries
each follicle has theca + granulosa cells that surround and protect oocyte
Theca cells have LH receptors; when LH binds to theca cells ==> release Androstenedione
Granulosa cells have FSH receptors; when FSH binds to granulosa cells ==> Aromatase (enzyme)
Aromatase converts Androstenedione into estradiol
estrogen causes follicular growth
estrogen acts as negative feedback on hypothalamus + anterior pituitary to inhibit GnRH/ FSH / LH production
this negative feedback prevents another follicle from being stimulated by FSH, so only 1 egg released
the follicle with the most FSH receptors grows the quickest, and becomes the dominant follicle
the dominant follicle rise in estrogen now becomes positive feedback on GnRH / FSH / LH - this switch occurs 1-2 days prior to ovulation
the massive surge in LH causes rupture of ovarian follicle => release of oocyte (ovulation) –> luteal phase

PCOS = BEGINS IN THE FOLLICULAR PHASE

in PCOS = the anterior pituitary gland makes TOO MUCH LH, and NOT ENOUGH FSH
excess LH causes theca cells to produce excess amounts of androstenedione
not enough aromatase available from FSH/granulosa cells to convert androstenedione to estradiol

Aromatase is present in fat cells, therefore obese patients –> elevated estrogen

estrogen inhibits FSH
anovulation increases LH
the excess androstenedione enters the blood, is converted to testosterone
because LH levels are so high, there is no LH surge to trigger rupture of dominant follicle (ovulation)
may remain there in ovary as a cyst, or may degenerate with other follicles

Not well understood what causes the anterior pituitary to make so much LH

** MAJORITY OF PCOS = INSULIN RESISTANCE **
- thought that this somehow disrupts menstrual cycle
- insulin resistance = cells in liver, muscles and adipose tissue become insensitive to insulin, and therefore cannot pull glucose in from the blood
==> can develop into DM

The pancreas continues to secrete more and more insulin, despite insulin resistance
==> may develop hyperinsulinemia

Theca cells (LH) have insulin receptors; so excess insulin can bind to theca cells, causing them to grow and divide --> too many LH receptors
- so thought that this is what causes GnRH to release excess amounts of LH, and lack of surge therefore prevents regular ovulation

SYMPTOMS OF PCOS
- High levels of Androstenedione (from Theca / LH) ==>
⦁ Hirsutism (excess hair growth)
⦁ thinning of hair (male pattern baldness)
⦁ acne

lack of ovulation
⦁ amenorrhea (no periods) or oligomenorrhea (infrequent or irregular periods)
chronic anovulation ==> infertility
but due to excess estrogen, when periods do occur = heavy + painful
insulin resistance
⦁ overweight / obese
⦁ type II DM
⦁ acanthosis nigricans

TRIAD

1) amenorrhea (chronic anovulation) / oligomenorrhea
2) obesity
3) hirsutism (androgen excess)
- PCOS due to insulin resistance*

INCREASED RISK FOR
⦁ breast cancer
⦁ endometrial cancer

Along with an increased risk for breast carcinoma, hyper-estrogenism in PCOS can increase the risk of endometrial hyperplasia, which is a precursor to endometrial carcinoma.
- unopposed estrogen –> endometrial hyperplasia

DIAGNOSIS OF PCOS
⦁ high ratio of LH to FSH (>/= 3:1)
- high LH, low FSH
⦁ elevated androstenedione, elevated testosterone
⦁ elevated estrogen
⦁ hyperinsulinemia
⦁ Ultrasound - cysts on ovaries - “beading” or “string of pearls” (but not necessary to diagnose PCOS)

ROTTERDAM CRITERIA - requires 2/3
⦁ oligomenorrhea / anovulation
⦁ hyperandrogenism (clinical or biochemical)
⦁ polycystic ovaries on ultrasound

TREATMENT
⦁ weight loss through diet + exercise = can help reduce insulin resistance
⦁ OCPs (help regulate menstrual cycle) = 1ST LINE
⦁ Spironolactone = anti-androgenic properties
⦁ Clomid (clomiphene) - induces ovulation
⦁ metformin (increases insulin sensitivity)

Patient will present as → a 13 year old girl who is overweight has her first menses at age 13 and then has no menses until she is 16 and then has another menstrual period 6 weeks later. Ultrasound shows enlarged cystic ovaries with a string of pearls on ultrasound. LH to FSH ratio is 3:1

Question 10

Q

ECTOPIC PREGNANCY (or tubal pregnancy)

Answer

A

“ectopic” = out of place

so Ectopic Pregnancy = pregnancy that is somewhere other than the uterine cavity

In order for an ectopic pregnancy to take place:

1) egg is fertilized and is implanted somewhere other than the endometrium of the uterine cavity
2) must implant on a surface with enough rich blood supply to support a developing embryo

ECTOPIC PREGNANCIES CAN OCCUR
⦁	Fallopian Tube (MC)
 - the ampulla of fallopian tube = MC location in tube
⦁	Ovaries
⦁	Intestine

After implantation, the embryo starts developing the way it normally would in the uterine cavity

OVER TIME, THE FOLLOWING CAN HAPPEN
1) tissue can no longer supply a sufficient blood supply for the embryo ==> eventually dies

2) if tissue can provide adequate blood supply, then hormones from the corpus luteum + placenta ==> missed menstrual period, nausea, breast enlargement (all symptoms seen in early pregnancy)

If implantation was in ampulla of fallopian tube, the embryo eventually runs out of space ==> stretches the nerve fibers within the wall of fallopian tube ==> LOWER ABDOMINAL PAIN
- can eventually rupture the fallopian tube

A ruptured ectopic pregnancy can lead to:
⦁ massive hemorrhaging into abdominal cavity
⦁ blood can irritate the peritoneum, which can cause ** REFERRED PAIN TO SHOULDER **
⦁ light vaginal bleeding

Internal bleeding + severe pain + damage to fallopian tube ==> MEDICAL EMERGENCY

CAUSE OF ECTOPIC PREGNANCY
⦁ unknown

RISK FACTORS
⦁	smoking
⦁	hx of PID
⦁	in-vitro fertilization
⦁	gynecologic surgery
⦁	current IUD
⦁	tubal ligation
⦁	previous hx of ectopic pregnancy
⦁	hx of infertility
⦁	gestational diabetes
⦁	DES exposure

Kartagener (primary ciliary dyskinesia) syndrome is a syndrome with immotile cilia due to a dynein arm defect that results in infertility and an increased risk of ectopic pregnancy.

SYMPTOMS
⦁	Amenorrhea
⦁	Abdominal / Pelvic pain
⦁	Vaginal bleeding
⦁	may have nausea / breast enlargement
⦁	may have fever

CLASSIC TRIAD of ectopic pregnancy =

1) abdominal pain
2) amenorrhea
3) vaginal bleeding

Other symptoms of ectopic pregnancy may be related to early pregnancy (nausea, breast fullness, constipation)

or symptoms of ectopic rupture (hemodynamic instability, dizziness or weakness, fever, vomiting, tachycardia, hypotension) which warrants urgent surgical treatment!!

The major risk of ectopic pregnancy is severe hemorrhage, which can lead to hypovolemic shock, and eventually death.

Typically develop pelvic pain around 6-8 weeks into pregnancy if implantation is in fallopian tube

If implantation occurs where there is much more space available ==> pain and bleeding may not occur until several weeks later

Ectopic pregnancy is often clinically mistaken for appendicitis as presenting symptoms of pain, nausea, and fever are shared between the two.

A PSEUDOSAC is a collection of fluid within the endometrial cavity created by bleeding from the decidualized endometrium = is often associated with an ectopic pregnancy.

PHYSICAL EXAM
⦁ may have palpable mass near uterus
⦁ abdominal tenderness
- but these symptoms mimic a normal pregnancy - which can contribute to a delay in diagnosis

DIAGNOSIS
⦁ first - patient needs to be hemodynamically stable = vital signs in normal range, no hypotension or tachycardia

If hemodynamically unstable = IMMEDIATE SURGERY for both diagnosis + treatment

If hemodynamically stable
⦁ first = urine pregnancy test
⦁ serial hcg testing = check to see that levels are doubling every 2 days = typical in an early pregnancy
- normally double every 24-48 hrs

Compared to a normal pregnancy, hcg is DECREASED in ectopic pregnancy

⦁ Transvaginal ULTRASOUND- to check for intrauterine pregnancy = visible by week 5-6
** may see FREE FLUID in abdomen ** = blood = ruptured ectopic pregnancy

Transvaginal ultrasound is safe and commonly performed during all stages of pregnancy, including the first trimester
- The transabdominal ultrasound is not as sensitive for the detection of a gestation sac or fetal heartbeat compared with transvaginal ultrasound

* gestational sac should be visualized on transvaginal US when serum ßhCG levels reach 1,500-2,000 IU/L or when transabdominal US reaches 3600 mIU/ mL with abdominal ultrasonography.* (4.5-5weeks)

A TUBAL RING is an echogenic, ringlike structure found outside of the uterus on ultrasonography, that represents an early ectopic pregnancy.
“ring of fire” = doppler ultrasound

If transvaginal ultrasonography does not show an intrauterine pregnancy when the β-hcg levels are reached, the pregnancy can be considered ectopic.

Ectopic = Beta HCG is > 1,500, but no fetus in utero

TREATMENT
o if patient is hemodynamically stable, diagnosed early, and hcg levels are already declining
⦁ may not need any additional treatments / procedures - can continue to monitor via serial hcg

if diagnosed later (≤ 8 weeks) + hemodynamically stable
⦁ Methotrexate IM - can be used to terminate the pregnancy

MTX requires careful patient selection and is most successful in patients with a b-hCG is <5000 IU/L, and a gestational sac <3.5cm, and no pulmonary, renal or hepatic disease
- monitor on days 0, 4, 7 (b-hcg should drop by 15%+ by day 4-7)

Methotrexate is the standard medication used in the treatment of an unruptured ectopic pregnancy.

Methotrexate is a folic acid analog that competitively inhibits dihydrofolate reductase and is used to treat ectopic pregnancy and medical abortion

if hemodynamically unstable = EMERGENT SURGERY!
⦁ salpingostomy = open fallopian tube, remove pregnancy, close
⦁ salpingectomy = removal of fallopian tube (laparoscopic or open)

Surgical management is indicated for any patient who is medically unstable, is hemorrhaging, has a gestational sac >3.5cm, or a higher b-hCG level (making medical management is more likely to fail)
- if MTX doesn’t work = surgery

GIVE RHOGAM IF MOTHER IS Rh-

Use contraception x at least 2 months

Patient will present as → a 22-year-old female complaining of severe left lower quadrant abdominal pain associated with some spotting. She is sexually active, does not use contraception, and has a history of PID. She denies being pregnant. Her last period was 9 weeks ago. On physical exam, the patient is hypotensive and tachycardic. A vaginal ultrasound is performed demonstrating free fluid and a mass in the right adnexa.

TRIAD = LOWER ABDOMINAL PAIN + AMENORRHEA + VAGINAL BLEEDING
(also seen with threatened abortion, but will have open os)

Question 11

Q

HCG LEVELS DURING PREGNANCY

Answer

A

⦁ 1-3 weeks LMP: 5 – 50 mIU/mL
⦁ 4 weeks LMP: 5 – 426 mIU/mL
⦁ 5 weeks LMP: 18 – 7,340 mIU/mL
⦁ 6 weeks LMP: 1,080 – 56,500 mIU/mL
⦁ 7 – 8 weeks LMP: 7, 650 – 229,000 mIU/mL
⦁ 9 – 12 weeks LMP: 25,700 – 288,000 mIU/mL
⦁ 13 – 16 weeks LMP: 13,300 – 254,000 mIU/mL
⦁ 17 – 24 weeks LMP: 4,060 – 165,400 mIU/mL
⦁ 25 – 40 weeks LMP: 3,640 – 117,000 mIU/mL

Non-pregnant females: 0 – 5 mIU/mL

Postmenopausal females: 0 – 8 mIU/mL

These numbers are just a guideline – every woman’s level of hCG can rise differently. It is not necessarily the level that matters, but rather the change in the level.

A low hCG level can mean any number of things and should be rechecked within 48-72 hours to see how the level is changing.

A low hCG level can indicate:
⦁ Miscalculation of pregnancy dating
⦁ Possible miscarriage or blighted ovum
⦁ Ectopic pregnancy

A high level of hCG can also mean a number of things and should be rechecked within 48-72 hours to evaluate changes in the level.

A high hCG level can indicate:
⦁ Miscalculation of pregnancy dating
⦁ Molar pregnancy
⦁ Multiple pregnancy

Beta-hCG is secreted from the time of implantation and is detectable about 7–8 days after fertilization

Question 12

Q

PRE-ECLAMPSIA

Answer

A

a condition that affects pregnant women
occurs after 20 weeks gestation
in some cases, can develop up to 6 weeks after delivery

MC occurs in final trimester

CLINICAL MANIFESTATIONS
⦁ New onset Hypertension
⦁ Proteinuria (marker of kidney damage)
⦁ can cause damage to other organs as well (such as brain + liver)

HYPERTENSION + PROTEINURIA

WIDE-RANGE OF SYMPTOMS
⦁ asymptomatic or mild vs life-threatening

PREECLAMPSIA + SEIZURES = ECLAMPSIA***

RISK FACTORS FOR PREECLAMPSIA
⦁  first pregnancy
⦁  multiple gestation (twins / triplets / etc)
⦁  mothers > 35
⦁  hypertension
⦁  diabetes
⦁  obesity
⦁  family hx of preeclampsia

PATHOPHYSIOLOGY
Cause = develop of an abnormal placenta

Normally in pregnancy, spiral arteries dilate to 5-10x their size and develop into large utero-placental arteries in order to deliver large quantities of blood to the developing fetus

1) UTERO-PLACENTAL ARTERIES BECOME FIBROUS / NARROWED
- In Pre-eclampsia, these utero-placental arteries become fibrous –> narrow, so less blood gets to the placenta
- a poorly perfused placenta can lead to intrauterine growth restriction + even fetal death

2) HYPO-PERFUSED PLACENTA RELEASES PRO-INFLAMMATORY PROTEINS-
- Placenta is hypo-perfused –> releases pro-inflammatory proteins
- these proteins enter maternal circulation –> cause the damage to endothelial cells that line blood vessels –> become dysfunctional

3) ** DAMAGED ENDOTHELIAL CELLS ** IN BLOOD VESSELS
- causes vasoconstriction
- also causes kidneys to retain more sodium
- -> Hypertension!

** VASOCONSTRICTION + SODIUM RETENTION IN KIDNEYS –> HYPERTENSION **

4) ** MATERNAL VASOSPASM **
- pro-inflammatory proteins can also cause local vasospasm, and therefore start to affect specific organs

⦁ reduced blood flow to kidneys –> glomerular damage –> oliguria (decreased urine output) + proteinuria (sign of glomerular damage)

⦁ reduced blood flow to retina –> blurred vision / flashing lights / scotomas (blurry spot in vision)

⦁ reduced blood flow to liver –> severe liver injury + swelling –> elevated LFTs + stretches the capsule around the liver –> RUQ pain

5) MICRO-THROMBI FORMATION IN VASCULATURE
- Endothelial cell injury leads to formation of lots of tiny thrombi in micro-vasculature
- uses up lots of platelets –> thrombocytopenia ± DIC
- as RBCs try to navigate around clots in vessels, eventually run into clots and lyse –> hemolysis –> HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets)

HELLP syndrome develops in 10-20% of patients with severe pre-eclampsia / eclampsia

6) INCREASED VASCULAR PERMEABILITY
- endothelial damage increases vascular permeability ==> water leaks out of vessels and into tissues
- due to lack of protein in blood from proteinuria, there is lower osmotic pressure in vessels, so even more fluid leaks out of vasculature into tissues
==> Generalized Edema (legs / face / hands)
==> Pulmonary Edema (cough / SOB)
==> Cerebral Edema (headaches / confusion / seizures)

PRESENCE OF SEIZURES = NOW ECLAMPSIA

CLASSIC TRIAD OF PRE-ECLAMPSIA

1) Hypertension
2) Proteinuria
3) Edema

must have HTN + proteinuria to diagnose preeclampsia

Preeclampsia is caused by abnormal placental spiral arteries leading to endothelial dysfunction, vasoconstriction and ischemia.

POSSIBLE SYMPTOMS
⦁  HTN
⦁  proteinuria
⦁  edema
⦁  headache
⦁  visual symptoms
⦁  oliguria
⦁  confusion
⦁  cough
⦁  SOB
⦁  thrombocytopenia

DIAGNOSIS OF PRE-ECLAMPSIA
⦁ Systolic BP > 140mmHg
⦁ Diastolic BP > 90mmHg

o Mild Preeclampsia = BP ≥ 140/90
⦁ Proteinuria: > 300mg/24 hours or +1 on dipstick

The diagnosis of mild preeclampsia requires 2 serial blood pressure readings of >140/90 mmHg over 6 hours or more, and > 0.3 g/24hrs of protein in the urine.

o Severe pre-eclampsia = BP ≥ 160/110
⦁ Proteinuria: > 500mg/24 hours or +3 on dipstick
- these extreme BPs can lead to hemorrhagic stroke or placental abruption (placenta prematurely detaches from uterine wall)

Preeclampsia is considered severe with blood pressure of >160/110 mmHg, urinary protein of >0.5g/day, or if there are signs of end-organ damage such as visual disturbance, hepatocellular injury, thrombocytopenia, oliguria (<500mL produced per day), fetal growth restriction, or pulmonary edema.

⦁ Oliguria = < 500mL/day

Abdominal pain, nausea, retrosternal chest pain, and headache are common symptoms of preeclampsia with severe features

COMPLICATIONS
- Patients who have had preeclampsia have increased risk of developing 
⦁  hypertension later in life 
⦁  ischemic heart disease
⦁  stroke
⦁  venous thromboembolism.

TREATMENT
o Mild Pre-eclampsia
⦁ DELIVERY OF FETUS + PLACENTA**
- depends on gestational age + severity of disease

Delivery at 37 weeks gestation
May deliver at 34-36 weeks if necessary

- If < 34 weeks = Conservative treatment
⦁     daily weights
⦁     weekly BP
⦁     weekly dipstick
⦁     bedrest

If < 34 weeks = STEROIDS to mature lungs (betamethasone)

o Severe Pre-eclampsia
⦁ DELIVERY OF FETUS + PLACENTA**
- prompt delivery = only cure + Hospitalization

⦁ *** MAGNESIUM SULFATE * to prevent eclampsia (seizures) - can be given x 24-48 hours
⦁ BP MEDS if severe HTN = HYDRALAZINE
(others = labetalol, nifedipine)

If symptoms develop after delivery, treatment = manage symptoms, which will slowly subside on their own

Sodium nitroprusside is a medication used in severe hypertensive emergency in pregnancy, where first-line medications have failed to lower the blood pressure.

Question 13

Q

ECLAMPSIA

Answer

A

ECLAMPSIA = Pre-eclampsia + SEIZURES or COMA

= life threatening for mother + fetus

SYMPTOMS
⦁     abrupt tonic-clonic seizures x 1-2 min followed by post-ictal state
- may have
⦁     headache
⦁     visual changes
⦁     cardiorespiratory arrest

Patient meets all criteria for preeclampsia (HTN + Proteinuria + Seizures or Coma)

PREECLAMPSIA + SEIZURES = ECLAMPSIA***

RISK FACTORS FOR PREECLAMPSIA / ECLAMPSIA
⦁  first pregnancy
⦁  multiple gestation (twins / triplets / etc)
⦁  mothers > 35
⦁  hypertension
⦁  diabetes
⦁  obesity
⦁  family hx of preeclampsia

PATHOPHYSIOLOGY
Cause = development of an abnormal placenta