Gynecology Flashcards
Etiology abnormal uterine bleeding
PALM-COIN
Polyp Adenomyoma Leiomyoma (fibroid) (MCC perimenopausal) Malignancy (MCC post-meno after atrophic endometrium) Coagulopathy Ovulatory dysfunction (MCC 15-19) Endometrial Iatrogenic Not yet classified
MCC abnormal uterine bleeding by age
Overall = PREGNANCY
Infants- 2/2 estrogen withdrawal, normal
After neonate, before puberty - always abnormal - urethral prolapse, infection, saddle injury, abuse
After puberty - pregnancy, anovulatory bleeding, hyper-prolactinemia, PCOS, hypothyroid
19-30 YO Structural (PALM), pregnancy, OCP use, endometrial issue
Post-menopausal - ALWAYS ABNORMAL - Atrophic endometrium vs cancer
What is anovulatory bleeding? Treatment
When you don’t ovulate/release egg during one menses cycle
Physiology: Normally ovulation triggers progesterone production. Lack in progesterone from an anovulatory cycle = abnormal bleeding - may be mistaken for normal period but can last >7 days
Treatment: Observe & reassure if 16-19. OCPs/IUD if pregnancy not desired. Pregnancy desired - short term progestin (norethidrone). Super heavy bleeding - admit
Refractory bleeding - think coagulopathy
Uterine polyp - sx, dx, tx
Abnormal uterine bleeding - P in PALM-COIN
CP: ASX bleeding BETWEEN periods (metrorrhagia) and after heavy lifting
Dx: Histologically
Tx:
ASX & low risk CA - leave
Seeking fertility or large - remove
Causing sx or inc risk CA (pos-menopausal) - remove
Removed via hysteroscopy - want to visualize the inside of the uterus to see if any other lesions - need histology report to see if it was cancerous
Post-menopausal bleeding workup
- Inspect - bleeding, ulcers, lesions? Pap smear
- Transvaginal US - measures endometrial thickness
- < 4mm low risk CA, >4mm - sonohysterogram (inject fluid into uterus, see if focal or global thickness)
- Focal thickness - hysteroscopy w/ Bx. Global thickness - Endometrial bx +/- D&C
- Bx results - w/ atypia - hysterectomy. W/o atypia IUD, noethindrone, medroxyprogesterone
MCC AUB 19-39 YO
Uterine polyp
12-19 YO MCC AUB
Anovulatory cycles 2/2 immature HPO axis
Workup of AUB
Pregnancy test CBC Thyroid function tests Coags Cervical cx (esp w/ post-coital bleeding)
Ultrasound - can show IUP, endometrial thickness, ectopic preg, adnexal mass
Sonohysterography - shows polyps, subserous leiomyomas (fibroids), adenomyomas
Abnormal pap –> colposcopy w/ Bx & EC
Estrogen free contraceptive methods - when given? List methods available
Given to postpartum women - can’t have estrogen = more clots & gets in breast milk. >35 YO & smokes estrogen C/I bc of clots. Stroke, migraine w/aura, VTE, current breast CA, coagulopathy
IUD (C/I active infection, didephyls)
Progesterone only pills (postpartum)
Depo-Provera (deprives of fertility, pro only)
Nexplanon (irregular bl, not if change wt)
Copper IUD
Disadvantages copper IUD
Heavy menses
Dysmenorrhea
C/I to IUD
Distortion of uterine cavity, active infection, pregnancy, PP sepsis, undiagnosed uterine bleeding
Disadvantages Nexplanon
Big weight change = difficult removal
Irregular bleeding patterns in some
BBW Transdermal patch
BLOOD CLOTS
Therefore cannot give to pt w/ inc risk clots!!! (Smokers, prior Hx)
Also less effective in obese (dec ab)
Which contraceptive method has BBW for blood clots?
Transdermal patch
Do NSAIDs decrease or increase menorrhagia?
Decrease
MCC AUB postmenopausal
Atrophic endometrium Endometrial proliferation/hyperplasia Endometrial or cervical cancer Unopposed estrogen HRT or HRT w/ progesterone Atrophic vaginitis Trauma Endometrial polyps Friction ulcers 2/2 prolapse
What impact do thyroid hormones have on menstruation? AKA why is TFTs a part of the workup of amenorrhea?
Thyroid produces hormones that regulate metabolism - can impact the HPO axis!
Elevated TRH makes the pituitary gland secrete more prolactin….prolactin in turn INHIBITS GnRH!
No GnRH = NO FSH/LH = NO OVULATION!!!
Therefore MUST check TFTs as part of any ovulation workup
Thyroid issues can also cause pregnancy loss & complications in fetal development because of this.
The follicular phase of the ovarian cycle corresponds to the proliferative or secretory phase of the uterine cycle?
Proliferative
During second half of ovarian follicular phase is when the endometrium of the uterus is proliferating in preparation for the implantation of an egg
The luteal phase of the ovarian cycle corresponds to the proliferative or secretory phase of the uterine cycle?
Secretory
After ovulation, the progesterone produced by the CL stabilizes the endometrium of the uterus. This part of the uterine cycle is known as the secretory phase (name is kind of a misnomer - makes it sound like your menstruating here but you’re not yet. Called secretory phase because progesterone stimulates endometrium secretory cells to secrete mucus - prevents penetration of another sperm)
IF no implantation of egg, the CL degenerates and progesterone falls, then your endometrium degenerates & a few days later start menstruating = day 1 of cycle and day 1 of follicular phase
A 15 year old presents to your primary care office stating she has never had her period - on exam you notice she is short in stature, has a webbed neck, and wide-spaced nipples - what is the most likely cause of her amenorrhea?
Turner syndrome - causes amenorrhea & infertility but can also be a/w coarctation of the aorta = not safe to carry a pregnancy
Primary armenorrhea vs secondary amenorrhea?
Primary - woman has NEVER had a period in her entire life
Age 15 if has 2nd sex characteristics. Age 13 if NO 2nd sex characteristics.
Secondary is you’ve had one or more menses but stopped having periods for >3 cycles or if periods are irregular than no menses for > 6 cycles (months)
Etiology of primary amenorrhea
> 50% caused by genetic and anatomic abnormalities!!!
Mnemonic - MOD-(ified) PATH to pregnancy
Mullerian agenesis (15%) Ovarian (gonadal) dysgenesis (43%) Delay of puberty (15%) - PCOS (more commonly 2nd amen) Anorexia nervosa/weight loss Transverse vaginal septum Hypopituitarism Hyperprolactinemia/prolactinoma GnRH deficiency
Gonadal (ovarian) dysgenesis
Gonadal (Ovarian) dysgenesis (43%) of primary amenorrhea
- Full w/ normal karyotype (46XY -Swyer syndrome, 46XX), partial, or turner (45, X0)
- Gonadal dysgenesis is classified as any congenital developmental disorder of the reproductive system in the male or female. It is the defective development of the gonads in an embryo, with reproductive tissue replaced with functionless, fibrous tissue, termed streak gonads
46 XY gonadal dysgenesis = Swyer syndrome. Rare. Swyer syndrome, or XY gonadal dysgenesis, is a type of hypogonadism in a person whose karyotype is 46,XY. The person is externally FEMALE with streak gonads, and if left untreated, will not experience puberty
Genotypically MALE karyotype. But defect so that not expressed. Have uterus, FT, etc, but gonads are not functional & are fibrotic. Can become cancerous later in life, should be surgically removed as child. Must begin HRT in adolescence to induce any female secondary sex characteristics. So presents as primary amenorrhea w/ absence of pubarche and thelarche as well!!
Mullerian agenesis
Mullerian agenesis (15%) of primary amenorrhea
- Congenital malformation characterized by a failure of the Müllerian duct to develop, resulting in a missing uterus and variable degrees of vaginal hypoplasia of its upper portion
Etiology secondary amenorrhea
Ur HPPOO = MESSED UP! Uterine (7%) r Hypothalamus (35%) PREGNANCY Pituitary (17%) Ovarian (40%) Other (1%)
Examples of hypothalamic dysfunction in secondary amenorrhea
BFTP: Etiology 2nd amen: Ur HPPOO = MESSED UP! Uterine (7%) r HYPOTHALAMUS (35%) PREGNANCY Pituitary (17%) Ovarian (40%) Other (1%)
Examples of hypothalamic dysfunction:
Functional hypothalamic amenorrhea (STRESS, OVER-EXERCISE, ANOREXIA - stress = CORTISOL which SHUTS DOWN GnRH secretion!!!)
Isolated GnRH deficiency
Other - systemic illness
Examples of pituitary dysfunction in secondary amenorrhea
BFTP: Etiology 2nd amen: Ur HPPOO = MESSED UP! Uterine (7%) r Hythalamus (35%) Pregnancy PITUITARY (17%) Ovarian (40%) Other (1%)
Examples of pituitary dysfunction in 2nd amen:
Prolictinoma
Hyperprolactinemia
Other sellar masses
Examples of ovarian dysfunction in secondary amenorrhea
BFTP: Etiology 2nd amen: Ur HPPOO = MESSED UP! Uterine (7%) r Hypothalamus (35%) PREGNANCY Pituitary (17%) OVARIAN (40%) Other (1%)
Examples of ovarian dys in 2nd amen: Turner syndrome (45X0) 46 XY gonadal dysgenesis Primary ovarian insufficiency (POI) - menopause<40YO Ovarian tumors PCOS
Swyer Syndrome
Swyer syndrome = gonadal (ovarian) dysgenesis = technically male karyotype (46XY) but have uterus, FT, just no gonads (ovaries) so no estrogen, progesteron = no 2nd sex characteristics etc
Rare. Genotypically male karyotype. But there’s a genetic defect so that XY not expressed correctly. Have uterus, FT, etc, but gonads are not functional & are fibrotic. Can become cancerous later in life, should be surgically removed as child. Must begin HRT in adolescence to induce any female secondary sex characteristics. So presents as primary amenorrhea w/ absence of pubarche and thelarche as well!!
PCOS
Ovaries have increased androgen production which arrests the growth of the follicles so the proliferative phase is not followed by a secretory phase.
Inc androgen stops dev, no ovulation occuring. Ov dys = si/sx. Hirsutism, acne, increased hair growth. Have insulin resistance, overweight. PCOS have to have one of two following criteria:
- PC ovaries on US
- Si/sx hyperandrogenism (Overweight/obese w/ insulin resistance/acne/hirsutism/hair)
- Oligomenorrhea (long cycles, go >35 days, lots of annovulatory cycles etc) or amenorrhea (uncommon, but if happens = secondary) typically not first presenting sx of PCOS –> tough dx to make sometimes, differing presentations
More often oligomenorrhea. Therefoe more often secondary not primary amen.
Note: Polycystic ovaries does not mean PCOS. Must meet 2/3 criteria (hyperandrogenism –> measure testosterone or look for signs, also Polycystic ovaries on US & oligomenorrhea/amenorrhea
What is Asherman syndrome?
AKA IUA (intrauterine adhesions) = Scarring of uterus or endometrium. Secondary. Not at birth. Caused by post-partum hemorrhage, infection of endometrium etc
There isn’t any one cause of AS. Risk factors can include myomectomy, Cesarean section, infections, age, genital tuberculosis, and obesity
Uterine causes of secondary amenorrhea?
BFTP: Etiology 2nd amen: Ur HPPOO = MESSED UP! UTERINE (7%) r Hypothalamus (35%) PREGNANCY Pituitary (17%) Ovarian (40%) Other (1%)
Uterine causes of 2nd amen - more straight forward structural abnormalities
Intrauterine adhesions (asherman syndrome) - Scarring of uterus or endometrium. Secondary. Not at birth. Caused by post-partum hemorrhage, infection of endometrium etc
Mullerian agenesis - no uterus or no vagina 2/2 no mullerian duct development in utero
Imperforate hymen
Transverse vaginal septum
Primary amenorrhea workup
Look up up to date chart
Labs: Hcg, FSH, TSH, PRL & pelvic ultrasound to see if uterus is present
If no uterus –> order karyotyping (mullerian agenesis, complete androgen insensitivity syndrome (rare), 5-alpha-reductase deficiency)
If uterus present w/ HIGH FSH - think 46,XY gonadal dysgenesis
If uterus w/ normal development & normal FSH: structural abnormality (imperforate hymen, transverse vaginal septum) OR endocrine abnormality (high prolactin, abnormal TSH etc)
If uterus w/ normal FSH & NO 2nd sex dev –> repeat FSH and LH - if both low = congenital GnRH deficiency or delay of puberty. If LH low, FSH normal, then functional hypothalamic amenorrhea (stress, anorexia etc) or systemic illness - for either you need a pituitary MRI to rule out selar mass
Dysmenorrhea definition
Recurrent crampy lower abd pain that occurs on or near (DURING) menstruation in the absence of other pelvic pathology
DOES NOT HAPPEN MID-CYCLE
Dysmenorrhea etiology
Caused by excess production of endometrial prostaglandin = dysrhythmic uterine contractions - prostaglandins also stimulates the GIT so can have nausea, vomiting, diarrhea
Ddx dysmenorrhea
Adenomyosis Fibroids Endometriosis PID Miscarriage Ectopic Psychogenic
Tx dysmenorrhea
FIRST LINE = NSAIDS (decrease PGE!!!)
SECOND LINE = OCPS - (Note: Can also be considered first line for patients who are sexually active & want contraception as well)
PMS definition
Physical, emotional, behavioral, and cognitive symptoms that occur repetitively in the SECOND half of the menstrual cycle which RESOLVE after the onset of menses & interfere with some aspect of the woman’s life
This is the key difference between dysmenorrhea and PMS = timing
PMDD definition
Severe form of PMS which symptoms of anger, irritability, and internal tension are prominent
PMS/PMDD pathophysiology
Unknown but thought to be 2/2 hormonal changes ensuing after ovulation which affect the functioning of central neurotransmitters
Treatment of PMS/PMDD
1st line = SSRIs
2nd line = OCPs
3rd line = GnRH agonists w/ low dose estrogen progestin replacement (OCP)
4th line = surgery
Reasons why you cannot have estrogen
Recent pregnancy - hypercoagulable 6 weeks after
Family hx blood clots
Prior history of blood clots
> 35 & smoker (high risk clots)
Prior history of stroke, IHD, migraine w/ aura
Indication for OCPs
Menses regularity Tx menorrhagia, dysmenorrhea Menstrual migraine Tx acne/hirsutism To increase BMD Bleeding uterine fibroids Hypertension (>160/110)
Do OCPs increase or decrease the risk of endometrial , ovarian, and colorectal cancer?
Decreases
Can you breastfeed on OCPs?
NO YOU CAN NOT - estrogen gets into breast milk
Breast-feeding mothers MUST use progesterone-only birth control option
Progesterone-only birth control options
Oral progesterone only pills (given postpartum) Depo-Provera shots Copper IUD Hormonal IUD Nexplanon Female/male sterilization
Disadvantages of progesterone only pills
Short half life - MUST TAKE SAME TIME EVERY DAY
No suppression of follicular cysts
Irregular bleeding
Does less estrogen in OCPs cause more or less breakthrough bleeding? -when does the BTB occur in the cycle?
Less estrogen = more BTB on days 1-9 of the cycle
Which contraceptive method has a BBW and what is that BBW?
Transdermal patch has a BBW for blood clots & therefore you cannot to give it to smokers or people with increased risk of clots
Also - less effective in obese people (less absorption)
Does the Nuvaring have estrogen in it? What is one disadvantage of it?
Yes it does have estrogen
It causes increased vaginal discharge (think fb)
Cannot give if breastfeeding
9% failure rate
What are two important things to remember about Depo-provera injection regarding family planning and when giving to teens?
Depo-Provera = “deprive’ of fertility/bone density & “Pro” gesterone only
Return of fertility is delayed 6-12 months
Causes bone loss - so teens must supplement with Vitamin D & calcium
Also causes WEIGHT GAIN = bad for teen
When is a follow up appointment suggested after hormonal or copper IUD placed?
6 weeks - greatest time of ejection after a period
What 3 things do you have to consider before placing an IUD
No current infection (GC/Chlamydia) NOT PREGNANT Undiagnosed uterine bleeding Distortion of uterine cavity PP sepsis
Method of inhibiting pregnancy: IUD
Prevents implantation (thick cervical mucus & endometrial atrophy)
Method of inhibiting pregnancy: OCPs
Stops ovulation
Advantages to copper IUD
No hormones
Lasts 10-12 years
Can be used for emergency contraception
MOA: Not fully understood but copper ions create hostile environment for implantation, physically blocks implantation
Advantages copper IUD
Can be used as emergency contraception
Non-hormonal - good if older & can’t have any hormones
REALLY cheap
Male sterilization follow up care after the procedure
Appointment 3 months after for semen analysis - use backup method until that appointment
Methods of birth control that prevent ovulation
OCPs, Nexplanon, depo-provera, nuvaring
Methods of BC that prevent fertilization
Abstinence, coitus interruptus, fertility awareness, barriers (condoms, diaphragm, spermicide), sterilization
Methods of BC that prevent implantation
IUDs, emergency contraception
Advantage/disadvantage of IUD
Advantage: Lighter, shorter periods
DIsadvantage: Cannot be used to suppress ovarian cysts
What is HEELP Syndrome? When does it typically present?
HEELP = hemolysis, elevated liver enzymes, low platelets = severe manifestation/complication of preeclampsia
Typically presents > 26 weeks gestation
PMS - when do sx occur, what are risk factors, what age group is most affected, first line treatment?
Sx in LUTEAL PHASE. NO SX IN FOLLICULAR PHASE!!! (part of DSM-5 dx)
Smoking, obesity = RF
Women in 40’s most affected
First line tx = SSRI
Ovarian torsion RF definitive dx, MC US Finding, & CP
RF: Ov cyst > 4cm, prior pelvic surgery, hx tubal ligation, fertility treatments & pregnancy
DEFINITIVE dx = surgical (US w/ doppler showing NO flow is highly specific but doppler showing + flow does not rule out torsion b/c ovary has dual blood supply & may maintain some flow even in presence of torsion)
MC US finding: Enlarged, edematous ovary
CP: Severe, sudden onset, unilateral pelvic pain (R>L)
Age distribution ovarian torsion?
Bimodal - two ovaries to torse, two age groups common
15-30 & post-menopausal
MCC Ovarian torsion
Large adnexal cyst (>4cm) which causes ovary to fall over on itself & cut off blood supply
Screening for ovarian cancer
Ultrasound
CA-125 (Tumor marker is elevated in 50-90% of women with early ovarian cancer)
Risk factors for ovarian cancer
Advanced age
Family hx
Inc estrogen exposure:
Early menarche
Late menopause
Nulliparity
Protective factors ovarian cancer
Hormonal contraception
Tubal ligation
Hysterectomy
Tx ovarian cancer
Surgical excision and debulking of tumor burden
Chemotherapy
Which genetic mutations are a/w familial ovarian cancer syndrome?
BRCA1 and BRCA2
What is the most common cause of gynecological death?
Ovarian cancer
What is the strongest risk factor for the development of endometritis?
Cesarean section
RF & Clinical presentation endometritis?
RF: C-section, PROM >24 hrs, Stage 2 labor > 12 hrs, High # pelvic exams
CP: Foul-smelling lochia
Occurs 2-3d postpartum, uterine tenderness, leukocytosis, fever
Workup endometritis
Ultrasound to look for retained products of conception
Tx endometritis
Broad-spectrum abx (usually polymicrobial)
Clindamycin plus gentamycin
or ampicillin/sulbactam
First line abx therapy for endometritis?
Clindamycin & gentamycin
Fetal heart rate: Variable decel FHR monitor means?
Fetal Heart Rate: mnemonic
VEAL CHOP
Variable – Cord Compression
Early – Head Compression
Accelerations – Okay
Late – Placental Insufficiency
Early decel on FHR monitor means?
Fetal Heart Rate: mnemonic
VEAL CHOP
Variable – Cord Compression
Early – Head Compression
Accelerations – Okay
Late – Placental Insufficiency
Late decel on FHR monitoring = ?
Fetal Heart Rate: mnemonic
VEAL CHOP
Variable – Cord Compression
Early – Head Compression
Accelerations – Okay
Late – Placental Insufficiency
MC condition a/w placental abruption?
Maternal hypertension, including essential hypertension, gestational hypertension and preeclampsia.
4 T’s of PPH
Uterine ATony - MCC
Trauma to birth canal
ReTention
Coagulopathy or Thrombin d/o
Tx uterine atony
Treatment is uterine massage
Oxytocin
Prostaglandins
Surgery
Pregnancy category risk A
A: No risk in controlled human studies B. No risk in controlled animal studies C: Small risk in controlled animal studies D. Strong evidence of risk to fetus X: Very high risk to fetus
Pregnancy category risk B
A: No risk in controlled human studies B. No risk in controlled animal studies C: Small risk in controlled animal studies D. Strong evidence of risk to fetus X: Very high risk to fetus
Pregnancy category risk C
A: No risk in controlled human studies B. No risk in controlled animal studies C: Small risk in controlled animal studies D. Strong evidence of risk to fetus X: Very high risk to fetus
Pregnancy category risk D
A: No risk in controlled human studies B. No risk in controlled animal studies C: Small risk in controlled animal studies D. Strong evidence of risk to fetus X: Very high risk to fetus
Pregnancy category risk X
A: No risk in controlled human studies B. No risk in controlled animal studies C: Small risk in controlled animal studies D. Strong evidence of risk to fetus X: Very high risk to fetus
PID ROSH Facts
The most common presenting symptom is lower abdominal pain.
Patients may also develop fever, vaginal discharge, dyspareunia, or abnormal bleeding.
On physical examination, the patient typically has a fever and is tender on pelvic examination either in the lower abdomen over the uterus, on cervical motion, or in the adnexa.
The absence of cervical motion tenderness does not rule out PID and the CDC recommends empiric treatment for sexually active women presenting with lower abdominal pain and one of the following if no other cause is identified: cervical motion tenderness, adnexal tenderness, or uterine tenderness.
A pregnancy test should be included in the workup of all women of child-bearing age.
For outpatient management, patients are treated with ceftriaxone 250 mg IM followed by a 2-week course of doxycycline. Metronidazole is sometimes added to the regimen at the judgment of the clinician.
Classic US appearance of ovarian torsion?
Enlargement with a heterogenous stroma and peripherally displaced follicles
Note: Most common findings = increased ovairan size & abnormal position in relation to the uterus
CAN be completely normal in intermittent torsion
Risk factors for ovarian torsion
Ovarian mass (>4-5cm)= MOST important risk factor
Pregnancy
Ovulation induction
Prior torsion
Gold standard for ovarian torsion diagnosis?
Laparoscopy
What is the generic of Nexplanon implant?
Etonogestrol
Uterine fibroids are most common in which race?
African americans = MUCH more common - aka if given an african american patient with heavy vaginal bleeding, pick a uterine fibroid/leiomyoma!!!
What hormone abnormalities do you find in PCOS?
HIGH LH!!!
(2/2 abnormal GnRH pulsation release)
Think PCOS = 4 divided by 2 = LH
Serum androgens also elevated
Preferred treatment for trichomonas?
Metronidazole 2 g orally in a single dose
Alternatives:
2 g oral tinidazole in a single dose or
500 mg oral metronidazole twice a day for 7 days
Outpatient management PID
Ceftriaxone 250 mg IM followed by a 2-week course of doxycycline
Metronidazole is sometimes added to the regimen at the judgment of the clinician.
Cervical cancer screening women ages 21-29
Cytology alone every three years
Cervical cancer screening women aged 30-65
Cytology AND
HPV testing every 5 years
DO NOT just do HPV testing alone - need BOTH > 35 YO
What is the standard treatment for most breast cancers?
Breast-conserving therapy (lumpectomy) w/ sentinal lymph node biopsy
Followed by radiation therapy
+/- more adjuvant therapy depending on tumor and patient characteristics
RF Placental abruption
MCC HYPERTENSION
Other: Maternal trauma, smoking, prior placental abruption
Most classic finding placental abruption on ultrasound & other common findings
Most classic: Retroplacental hematoma
Other common: echogenic debris in amniotic fluid, placental thickening
NOT –> ULTRASOUND HAS POOR SENSITIVITY FOR PLACENTAL ABRUPTION AND NORMAL ULTRASOUND CANNOT RULE OUT AN ABRUPTION!!!
Diagnosis is CLINICAL and HIGH suspicion may be maintained for any woman with late pregnancy vaginal bleeding or abdominal pain in absence of bleeding (20% don’t have bleeding)
Complications of placental abruption
Placental or uterine insufficiency leading to late decelerations, fetal demise, maternal coagulopathy (DIC) and hemorrhagic shock
Endometritis treatment
POLYMICROBIAL = BROAD SPECTRUM
ADMIT & GIVE IV CLINDA & GENTAMYCIN
Hydatidiform mold is a/w which cancer?
Choriocarcinoma
Classic US finding hydatidiform mole?
“Bag of grapes”
“Snowstorm” appearance””
Uterine size > GA
CP Hydatidiform mole (gestational trophoblastic disease)
Vaginal bleeding Pelvic pressure/pain Uterine size > GA Hyperemesis gravidarum Preeclampsia < 20 wks gestation HTN < 20 wks gestation
Pathophys Hydatidiform mole (gestational trophoblastic disease)
Collective term for d/o that includes partial & complete mole, invasive mole, choriocarcinoma and placental site trophoblastic tumor - can be neoplastic or non-neoplastic
Neoplastic GTD includes invasive mole, choriocarcinoma, and trophoblastic tumors. Hydatidiform mole is the most common form of GTD
Gestational trophoblastic disease (GTD) is a term used for a group of pregnancy-related tumours. These tumours are rare, and they appear when cells in the womb start to proliferate uncontrollably. The cells that form gestational trophoblastic tumours are called trophoblasts and come from tissue that grows to form the placenta during pregnancy
RF molar pregnancy
Extremes of maternal age
History of previous mole
What is serum alpha fetoprotein used as a marker of?
Serum alpha-fetoprotein (C) is a serum marker used to evaluate for fetal body wall defects. Increased maternal serum alpha-fetoprotein (AFP) is associated with neural tube defects, abdominal wall defects, or other congenital anomalies. Low AFP is associated with trisomy 21
Is the risk of gestational trophoblastic neoplasia higher after a complete mole or a partial mole?
Complete mole
Treatment hydatidiform mole?
Suction D&C
Can also monitor serial quantitative b-hcg to make sure returns to undetectable levels
What is the most common form of breast cancer?
Infiltrating ductal carcinoma (70-80%)
Also the most common breast cancer among men
Which kind of breast cancer is more common in women with BRCA1 mutation?
Medullary carcinoma
More common in women w/ BRCA1 and in younger women
Screening for breast cancer guidelines - ACOG vs USPSTF?
ACOG: Start at 40 YO annually
USPSTF: Start at 50 YO, every 2 years
+ HPV infection in 32 YO w/ negative cytology report = next best step?
Repeat pap and HPV testing in 1 year
Don’t need to to colposcopy b/c just has presence of the virus, not significantly abnormal cellular changes
Therefore negative cytology does not require immediate colposcopy
Options for emergency contraception & when to give
Give ASAP but up to 5 days - efficacy decreases
What do you do if you miss two or more birth control pills in a pack?
Take one missed pill ASAP (discard other missed)
Continue taking remaining pills at usual time (even if it means you take 2 pills in day)
No emergency contraceptives needed (but consider if have had sex near fertile period (during first week of pill pack - day 7 is when you ovulate)
If pills missed at end of BC pack, can omit non-hormonal
How long do you have to use backup methods (condoms) when starting birth control?
On average 7 days for BC to get up & running fully
What is the most common benign breast disorder and who does it affect?
Fibrocystic breast disease
Women of reproductive age (MC 30-50)
Incidence increases w/ age but hormonally influenced
CP fibrocystic breast disease
WORST PRIOR to menstrual cycle (estrogen-dependent)
BILATERALLY SYMMETRICAL CYCLICAL breast pain and palpable nodular cysts that blend into surrounding breast tissue - no singular palpable mass (if so get US +/- FNA) - freely moving in regards to adjacent structures
KEY = lumpiness fluctuates WITH menstrual cycle
FibroCYSTIC = CYCLIC
Diagnosis/workup of fibrocystic breast disease
Equivocal or non-suspicious exam & about to have period- re-examine in 2 weeks during follicular phase of menstrual cycle (day 5-7) is best for diagnosing
Fibroadenoma etiology & epidemiology
Etiology not clear - E/P may be causative
MC in YOUNG women - age 10-30 YO
CP Fibroadenoma (name 5+ characteristics)
1-5 cm in size - can change but NOT in relation to menses
Increase in size with pregnancy however
Regress after menopause
Round /oval - hard & rubbery
Discrete & well-defined
Movable
Tx fibroadenoma
Reassurance & monitoring
Serial breast exam/ mammo
Excision if super painful/uncomfortable
Breast mastitis etio, CP, dx, tx
Etio: S. aureus
CP: u/l inflam/red/sore, fever/chills
Dx: hx current breastfeeding, correct CP - CAUTION if CP does NOT match classic mastitis b/c breast CA can mimic!!!
Tx: Dicloxacillin
Etiology of nipple discharge
Most are benign -
galactorrhea is white/clear
Can be pathologic -
Benign intraductal papilloma (MCC), drug-induced (methyldopa, imipramine, amphetamine, metoclopramide, OCP, etc), CNS - prolactinoma
or breast-cancer if blood-tinged
Characteristics of benign nipple discharge vs pathologic
Provoked, b/l, multi-ductal
Unilateral unprovoked discharge, uniductal, ANY BLOOD = BAD
Labs for nipple discarge
Pregnancy test, prolactin levels, thyroid function
Hormonal therapy for breast cancer?
(ER/PR positive breast CA) =
Tamoxifen (SERM) - 10 yrs
Aromatase inhibitors- 5yrs (anatrazole, aromasin)
ADR Tamoxifen
DVT, uterine cancer, vasomotor symptoms
ADR aromatase inhibitors
Less DVT/uterine CA than tamoxifen (SERM) but causes bone loss, myalgias, arthralgias
Contraindicated in pre-menopausal women
Which ER/PR positive breast cancer tx is contraindicated in pre-menopausal women?
Aromatase inhibitors (anatrazole, exemestane, letrozole)
TAMOXIFEN is what’s given in premnopausal women
Are aromatase inhibitors or SERM’s superior therapy for ER/PR positive breast CA patients?
Aromatase inhibitors are superior but contraindicated in premenopausal women…
MC breast disease 10-30
Fibroadenoma
MC breast disease 30-50
Fibrocystic disease
Breast lump > 50 YO
Breast CA until proven otherwise
Etiology syphilis
Treponema pallidium
CP Primary syphilis - incubation period?
Painless hard chancre (1 month after exposure)
Heals spontaneously after 1-2 months
CP Secondary syphilis, when does it occur?
Think of secondary as it spreading systemically = systemic symptoms
Fever, malaise, adenopathy, diffuse maculopapular rash (especially on palms and soles of feet), condyloma lata
Occurs 1-6 months after primary chancre
Fitz-Hugh-Curtis syndrome
PID & inflam of capsule around the liver (perihepatitis)
Woman will present with PID sx AND RUQ pain
Fitz-Hugh–Curtis syndrome is a rare complication of pelvic inflammatory disease (PID) involving liver capsule inflammation[1] leading to the creation of adhesions
Latent syphilis definition
Asymptomatic disease with serologic proof of infection - further classified as early latent (acquired w/in last year) vs late latent (acquired >1 year ago)
CP Tertiary syphilis
Occurs YEARS after primary infection
CP = Granulomas of the skin & bones (gummas), cardiovascular lesions (aortic aneurysms), neurosyphilis (tabes dorsalis, paresis, meningovascular disease)
Lymphogranuloma venereum etiology
C. trachomatis
CP neurosyphilis
= one of possibilities of tertiary syphilis
Presents as tabes dorsalis (gait abnormalities, paresthesias, weakness, tabetic gait (locomotor ataxia- feet slaps the ground), loss of coordination), paresis, meningovascular disease, +Rhomberg
Dementia, blindness
Existing nerve damage cannot be reversed
Lymphogranuloma venereum clinical presentation (three stages)
Primary lesion: Painless papule on genitals
Secondary stage: Inguinal lymphadenitis, fever, malaise, loss of appetite
Tertiary stage: Rectovaginal fistulas, rectal strictures
Lymphogranuloma venereum Diagnosis
NAAT, PCR
Lymphogranuloma venereum Treatment
100mg Doxy BID x 21 days
Think it’s a ton of sylables & it’s the a super long treatment
Treatment syphillis
Benzathine penicillin G
Which disease causes false positive RPR results?
Lupus
When do you begin suppressive therapy with anti-retrovirals if HSV positive and pregnant?
36 weeks
Active HSV outbreak in L&D?
Deliver via cesarean
Chancroid CP
SOFT papule –> PAINFUL genital ulcer
Gray, NON-indurated (syphilis is a HARD), gray base w/ ragged irregular edges
(Mnemonic - ducreyi - sounds like grey, people who cry are soft and need a rag (ragged edges) & they’re in pain - painful ulcer) - basically all the opposite of the syphilis ulcer
Inguinal lymphadenopathy
Incubation period chanroid
1 week
Treatment chancroid
AzithrOmycin
Think about how you treat haemophilis influenza w/ z-pak, treat haemophilis ducreyi w/ z-pak as well
+/- Ceftriaxone
Etiology chancroid
Haemophilus ducreyi
HaemO = ChancrO
Clinical Presentation cystocele
Feeling fullness, bulge from vagina (worse w/ standing),
Baden-walker classification of prolapse - Grade I
To the level of the ischial spines
Baden-walker classification of prolapse - Grade II
Between the ischial spines and the introitus
Baden-walker classification of prolapse - Grade III
Up to the introitus
Baden-walker classification of prolapse - Grade IV
Past the introitus
Risk factors for prolapse
Disturbing anatomical support (childbirth)
Increased abdominal pressure (cough- COPD, obesity, heavy lifting, chronic constipation)
Loss of levator ani function (postpartum)
Transection of supporting tissue: Post-surgical (hysterectomy)
Loss of innervation (ALS, paralysis, MS)
Atrophy of supporting tissues (post-menopausal)
Signs/symptoms of prolapse
Feeling of pressure/bulge Organ protrusion (esp w/ exertion) Incontinence Groin pain Dyspareunia Splinting to defecate
Symptom severity related to gravity - worse in evening/standing etc
Treatment prolapse
Asymptomatic - nonsurgical treatment - aka kegels, hormone/estrogen replacement therapy
Symptomatic - tx w/ pessary (especially useful with elderly or when surgery is contraindicated, surgery)
Indications for surgery - prolapse
When childbearing is completed and/or symptoms are interfering with patient’s functioning and do not respond to nonsurgical treatment
Complications of pelvic organ prolapse
Urinary retention Constipation Urinary tract infection Ulcerations Vaginal bleeding
Adenomyosis - pathophys
Ectopic endoetrial tissue within the myometrium - lining grows backwards into myometrium and causes hypertrophy and hyperplasia of the myoemtrium
Adenomyossis - CP
HUGE, THICK, “boggy” “globular” uterus
Not well differentiated from surrounding tissue so can’t exise well - why only definitive treatment is hysterectomy
Diagnosis adenomyosis
Can only be made pathologically
Can coexist with endometriosis and fibroids
Risk factors for adenomyosis
Parous women
Hx cesarean
Hx D&C
Average age of diagnosis adenomyosis
40-50 YO
Signs/sx adenomyosis
Menorrhagia (65%)
Dysmenorrhea (25%)
Chronic pelvic pain
Main Ddx for menorrhagia (heavy menstrual bleeding) (old-ish woman)
Uterine cancer
Leiomyoma
Adenomyosis
Polyps
Diagnosis of adenomyosis
Diagnosis only via histology s/p hysterectomy
Transvaginal ultrasound and MRI very helpful - MRI better but more expensive
TVUS / MRI “Key words” suspicious for adenomyosis
“Asymmetric thickening of myometrium”
“Linear striations” - from stretched tissue
“Loss of clear endo-myometrial border”
“Increased myometrial heterogeneity”
Treatment adenomyosis
Hysterectomy = only definitive treatment
Others try to treat the symptoms (bleeding & pain) -
OCPs/IUD - attempt to decrease bleeding and pain but not FDA-approved
GnRH analog - Lupron - decreases estrogen, may help /dysmenorrhea, menorrhagia
Aromatase inhibitor - prevents conversion of androgen to estrogen - less heavy bleeding & pain - CANNOT use forever
Endometriosis pathophys & CP
Presence of normal endometrial mucosa abnormally implanted in locations other than uterine cavity
ESTROGEN-dependent: The ectopic foci respond to cyclical hormonal fluctuations similar to intrauterine endometrium - = release of prostaglandins = inflammatory process = scarring of ectopic areas
Affects YOUNGER women than adenomyosis on average (25 YO - 40YO)
Types of functional ovarian cyst
Follicular cyst
Corpus luteal cyst
Theca lutein cyst
Endometrioma
Endometriosis diagnostic tools
TVUS but if don’t see anything helpful then only helped to rule out other bad stuff, didn’t help w/ dx of endometriosis
Definitive diagnosis = laparoscopy w/ bx - classic blue or black powder burned appearance
Ddx endometriosis
Appendicitis STD/PID UTI Ectopic pregnancy Primary dysmenorrhea Ovarian cysts
AKA LOTS OF PAIN
Endometriosis complications
Endometrioma - “chocolate cyst” - most common on ovaries
Adhesion formation
Pain
Infertility
Which GnRH agonist can induce pseudo-menopause to be used as treatment for heavy bleeding, painful periods caused by adenomyosis, endometriosis, fibroids etc?
Lupron
Only used for short period of time (6 month max) & if pt was not responsive to OCP tx
Side effects: Osteoporosis & menopause sx (hot flashes)
Endometriosis tx
95% will respond to medical management - OCPs, Lupron etc
If not effective, done w/ child-bearing = hysterectomy with BSO = considered the definitive tx
Simple cyst vs complex cyst
Simple: Fluid, thin wall (follicular, luteal, cystadenoma)
Complex: Debris, blood, thick wall, septations, hemorrhagic
Follicular cyst characteristics
Normally a mature follicle ruptures - if not it forms a cyst
Unilateral
Avg 3-8cm
Resolve spontaneously in 2-3 mo
70-80% resolve on their own
Follicular cyst ultrasound description
Simple, unilocular, UNILATERAL, anechoic (black, just fluid in there) cyst w/ thin, smooth wall
Corpus luteal cyst - when occur? Thin or thick-walled? simple or complex? Unilateral or bilateral? US description?
Occur after ovulation when normal CL would form
THICK walls, can be vascular
Can be simple or complex - inc likelihood of hemorrhagic cyst
Unilateral (only ovulate from one ovary at at time)
If vascular = “RING OF FIRE” APPEARANCE ON US
Theca lutein cyst - common or rare? Etiology? Unilateral or bilateral? Septations? Vascular?
Rare
Caused by ovarian hyperstimulation by bhcg - aka from gestational trophoblastic disease, hormonal therapy (from infertility treatment) - do not occur in regular singleton pregnancy - only in rare instances listed above, that’s why they’re rare
BILATERAL
No extra enhancement or blood flow on ultrasound but do have septations!
Endometrioma - AKA? age group? CP? Monitoring?
AKA “chocolate cyst - from endometrial tissue growing on ovaries in endometriosis - therefore the cyst is hormonally responsive
Age: Reproductive years when you’re ovulating & producing hormones
CP: Chronic pelvic pain (endometriosis presentation - dysparuenia, dyschezia, dysmenorrhea)
FU: Follow yearly w/ ultrasound or surgically remove
PCOS on ultrasound
“String of pearls”
> 10 PEIRPHERAL simple cysts
Benign ovarian tumors
Mature cystic teratoma (dermoid)
Cystadenoma
Cystadenofibroma
Complications of cysts and benign tumors
Ovarian torsion:
20-39 YO
Masses > 5cm
SUDDEN onset, sharp peain, the waxing/waining pain w/ n/v - goal is emergent surgery - time is ovary!
Hemorrhagic cyst:
Rupture w/ internal bleeding
Common w/ corpus luteal cysts on day 20-26 of cycle - their vascularity = bleeding risk
Persisten pain / pressure
Cystadenoma- serous
Benign ovarian tumor
25% are bilateral
PERI-menopausal women
Cystadenoma - mucinous
Can be very large
Age 20-40 (reproductive)
10% bilateral
Less frequent than serous cystadenoma
Cystadenofibroma - common or rare? Benign or malignant? Simple or complex? Age? Treatment?
Rare
Benign
Surface epithelial tumor - epithelium around ovary grows abnormally - resembles malignant tumor so must test
Complex cystic appearance to solid appearance
Ages 15-65
Tx: oophorectomy
Si/sx benign ovarian tumors and cysts
ASX
Pelvic pain
Fullness, heaviness, pressure, bloating
Irregular bleeding
Sudden/sharp pain –> ruptured cyst
Dx ovarian cysts/tumors
ULTRASOUND - distinguishes complex, simple, or solid
B-HCG
CA-125 (tumor marker for ovarian cancer, order in post-menopausal women w/ persistent cyst > 5cm)
Diagnostic laparoscopy
Management of cyst based on ultrasound results
Reproductive age
< 5 cm simple cyst
Observe
Management of cyst based on ultrasound results
Reproductive age
5-7 cm simple cyst
US follow up annually - make sure not rapidly enlarging
Management of cyst based on ultrasound results
Reproductive age
> 7 cm cyst
MRI or surgery for removal
Management of cyst based on ultrasound results
Post-menopausal
107 cm cyst
Ultrasound annually +/-
CA-125
Treatment of ovarian cysts
Analgesia management (NSAIDs)
OCPs - for recurrent functional cysts
Cystectomy if: Symptomatic Persisten 5-10cm cysts Ovarian torsion Suspected malignancy
Note: ** Surgery NOT required for follicular or corpus luteal cyst unless they are VERY large or hemorrhagic & have ruptured
Endometrioma
Initial f/u US in 6-12 weeks
and US annually vs
Cystectomy (see indications)
Indications for cystectomy
Symptomatic
Persistent 5-10cm cysts
Ovarian torsion
Suspected malignancy
Surgery (cystectomy) NOT required with….
Follicular or corpus luteal cyst unless they are VERY large or hemorrhagic & have ruptured
This is because they respond to OCPs well and most will resolve on their own without intervention
Treatment of ovarian cysts
Analgesia management (NSAIDs)
OCPs - for recurrent functional cysts
Cystectomy if: Symptomatic Persisten 5-10cm cysts Ovarian torsion Suspected malignancy
Note: ** Surgery NOT required for follicular or corpus luteal cyst unless they are VERY large or hemorrhagic & have ruptured
Si/Sx prolapse
Fullness/heaviness
NO PAIN
Inability to empty bladder fully, defecatory dysfunction
