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Gynecology Flashcards

1
Q

Etiology abnormal uterine bleeding

A

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
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2
Q

MCC abnormal uterine bleeding by age

A

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

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3
Q

What is anovulatory bleeding? Treatment

A

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

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4
Q

Uterine polyp - sx, dx, tx

A

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

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5
Q

Post-menopausal bleeding workup

A
  1. Inspect - bleeding, ulcers, lesions? Pap smear
  2. Transvaginal US - measures endometrial thickness
  3. < 4mm low risk CA, >4mm - sonohysterogram (inject fluid into uterus, see if focal or global thickness)
  4. Focal thickness - hysteroscopy w/ Bx. Global thickness - Endometrial bx +/- D&C
  5. Bx results - w/ atypia - hysterectomy. W/o atypia IUD, noethindrone, medroxyprogesterone
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6
Q

MCC AUB 19-39 YO

A

Uterine polyp

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7
Q

12-19 YO MCC AUB

A

Anovulatory cycles 2/2 immature HPO axis

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8
Q

Workup of AUB

A 
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

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9
Q

Estrogen free contraceptive methods - when given? List methods available

A

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

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10
Q

Disadvantages copper IUD

A

Heavy menses

Dysmenorrhea

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11
Q

C/I to IUD

A

Distortion of uterine cavity, active infection, pregnancy, PP sepsis, undiagnosed uterine bleeding

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12
Q

Disadvantages Nexplanon

A

Big weight change = difficult removal

Irregular bleeding patterns in some

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13
Q

BBW Transdermal patch

A

BLOOD CLOTS

Therefore cannot give to pt w/ inc risk clots!!! (Smokers, prior Hx)

Also less effective in obese (dec ab)

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14
Q

Which contraceptive method has BBW for blood clots?

A

Transdermal patch

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15
Q

Do NSAIDs decrease or increase menorrhagia?

A

Decrease

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16
Q

MCC AUB postmenopausal

A 
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
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17
Q

What impact do thyroid hormones have on menstruation? AKA why is TFTs a part of the workup of amenorrhea?

A

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.

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18
Q

The follicular phase of the ovarian cycle corresponds to the proliferative or secretory phase of the uterine cycle?

A

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

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19
Q

The luteal phase of the ovarian cycle corresponds to the proliferative or secretory phase of the uterine cycle?

A

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

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20
Q

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?

A

Turner syndrome - causes amenorrhea & infertility but can also be a/w coarctation of the aorta = not safe to carry a pregnancy

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21
Q

Primary armenorrhea vs secondary amenorrhea?

A

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)

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22
Q

Etiology of primary amenorrhea

A

> 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
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23
Q

Gonadal (ovarian) dysgenesis

A

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!!

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24
Q

Mullerian agenesis

A

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
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25
Q

Etiology secondary amenorrhea

A 
Ur HPPOO = MESSED UP! 
Uterine (7%) r 
Hypothalamus (35%)
PREGNANCY
Pituitary (17%)
Ovarian (40%) 
Other (1%)
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26
Q

Examples of hypothalamic dysfunction in secondary amenorrhea

A 
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

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27
Q

Examples of pituitary dysfunction in secondary amenorrhea

A 
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

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28
Q

Examples of ovarian dysfunction in secondary amenorrhea

A 
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
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29
Q

Swyer Syndrome

A

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!!

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30
Q

PCOS

A

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:

  1. PC ovaries on US
  2. Si/sx hyperandrogenism (Overweight/obese w/ insulin resistance/acne/hirsutism/hair)
  3. 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

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31
Q

What is Asherman syndrome?

A

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

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32
Q

Uterine causes of secondary amenorrhea?

A 
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

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33
Q

Primary amenorrhea workup

A

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

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34
Q

Dysmenorrhea definition

A

Recurrent crampy lower abd pain that occurs on or near (DURING) menstruation in the absence of other pelvic pathology

DOES NOT HAPPEN MID-CYCLE

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35
Q

Dysmenorrhea etiology

A

Caused by excess production of endometrial prostaglandin = dysrhythmic uterine contractions - prostaglandins also stimulates the GIT so can have nausea, vomiting, diarrhea

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36
Q

Ddx dysmenorrhea

A 
Adenomyosis
Fibroids
Endometriosis
PID
Miscarriage
Ectopic
Psychogenic
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37
Q

Tx dysmenorrhea

A

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)

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38
Q

PMS definition

A

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

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39
Q

PMDD definition

A

Severe form of PMS which symptoms of anger, irritability, and internal tension are prominent

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40
Q

PMS/PMDD pathophysiology

A

Unknown but thought to be 2/2 hormonal changes ensuing after ovulation which affect the functioning of central neurotransmitters

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41
Q

Treatment of PMS/PMDD

A

1st line = SSRIs
2nd line = OCPs
3rd line = GnRH agonists w/ low dose estrogen progestin replacement (OCP)
4th line = surgery

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42
Q

Reasons why you cannot have estrogen

A

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

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43
Q

Indication for OCPs

A 
Menses regularity
Tx menorrhagia, dysmenorrhea
Menstrual migraine
Tx acne/hirsutism 
To increase BMD
Bleeding uterine fibroids
Hypertension (>160/110)
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44
Q

Do OCPs increase or decrease the risk of endometrial , ovarian, and colorectal cancer?

A

Decreases

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45
Q

Can you breastfeed on OCPs?

A

NO YOU CAN NOT - estrogen gets into breast milk

Breast-feeding mothers MUST use progesterone-only birth control option

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46
Q

Progesterone-only birth control options

A 
Oral progesterone only pills (given postpartum) 
Depo-Provera shots
Copper IUD
Hormonal IUD 
Nexplanon
Female/male sterilization
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47
Q

Disadvantages of progesterone only pills

A

Short half life - MUST TAKE SAME TIME EVERY DAY
No suppression of follicular cysts
Irregular bleeding

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48
Q

Does less estrogen in OCPs cause more or less breakthrough bleeding? -when does the BTB occur in the cycle?

A

Less estrogen = more BTB on days 1-9 of the cycle

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49
Q

Which contraceptive method has a BBW and what is that BBW?

A

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)

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50
Q

Does the Nuvaring have estrogen in it? What is one disadvantage of it?

A

Yes it does have estrogen
It causes increased vaginal discharge (think fb)
Cannot give if breastfeeding
9% failure rate

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51
Q

What are two important things to remember about Depo-provera injection regarding family planning and when giving to teens?

A

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

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52
Q

When is a follow up appointment suggested after hormonal or copper IUD placed?

A

6 weeks - greatest time of ejection after a period

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53
Q

What 3 things do you have to consider before placing an IUD

A 
No current infection (GC/Chlamydia)
NOT PREGNANT 
Undiagnosed uterine bleeding 
Distortion of uterine cavity
PP sepsis
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54
Q

Method of inhibiting pregnancy: IUD

A

Prevents implantation (thick cervical mucus & endometrial atrophy)

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55
Q

Method of inhibiting pregnancy: OCPs

A

Stops ovulation

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56
Q

Advantages to copper IUD

A

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

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57
Q

Advantages copper IUD

A

Can be used as emergency contraception
Non-hormonal - good if older & can’t have any hormones
REALLY cheap

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58
Q

Male sterilization follow up care after the procedure

A

Appointment 3 months after for semen analysis - use backup method until that appointment

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59
Q

Methods of birth control that prevent ovulation

A

OCPs, Nexplanon, depo-provera, nuvaring

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60
Q

Methods of BC that prevent fertilization

A

Abstinence, coitus interruptus, fertility awareness, barriers (condoms, diaphragm, spermicide), sterilization

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61
Q

Methods of BC that prevent implantation

A

IUDs, emergency contraception

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62
Q

Advantage/disadvantage of IUD

A

Advantage: Lighter, shorter periods
DIsadvantage: Cannot be used to suppress ovarian cysts

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63
Q

What is HEELP Syndrome? When does it typically present?

A

HEELP = hemolysis, elevated liver enzymes, low platelets = severe manifestation/complication of preeclampsia

Typically presents > 26 weeks gestation

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64
Q

PMS - when do sx occur, what are risk factors, what age group is most affected, first line treatment?

A

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

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65
Q

Ovarian torsion RF definitive dx, MC US Finding, & CP

A

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)

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66
Q

Age distribution ovarian torsion?

A

Bimodal - two ovaries to torse, two age groups common

15-30 & post-menopausal

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67
Q

MCC Ovarian torsion

A

Large adnexal cyst (>4cm) which causes ovary to fall over on itself & cut off blood supply

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68
Q

Screening for ovarian cancer

A

Ultrasound

CA-125 (Tumor marker is elevated in 50-90% of women with early ovarian cancer)

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69
Q

Risk factors for ovarian cancer

A

Advanced age
Family hx

Inc estrogen exposure:
Early menarche
Late menopause
Nulliparity

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70
Q

Protective factors ovarian cancer

A

Hormonal contraception
Tubal ligation
Hysterectomy

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71
Q

Tx ovarian cancer

A

Surgical excision and debulking of tumor burden

Chemotherapy

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72
Q

Which genetic mutations are a/w familial ovarian cancer syndrome?

A

BRCA1 and BRCA2

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73
Q

What is the most common cause of gynecological death?

A

Ovarian cancer

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74
Q

What is the strongest risk factor for the development of endometritis?

A

Cesarean section

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75
Q

RF & Clinical presentation endometritis?

A

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

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76
Q

Workup endometritis

A

Ultrasound to look for retained products of conception

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77
Q

Tx endometritis

A

Broad-spectrum abx (usually polymicrobial)

Clindamycin plus gentamycin

or ampicillin/sulbactam

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78
Q

First line abx therapy for endometritis?

A

Clindamycin & gentamycin

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79
Q

Fetal heart rate: Variable decel FHR monitor means?

A

Fetal Heart Rate: mnemonic

VEAL CHOP

Variable – Cord Compression

Early – Head Compression

Accelerations – Okay

Late – Placental Insufficiency

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80
Q

Early decel on FHR monitor means?

A

Fetal Heart Rate: mnemonic

VEAL CHOP

Variable – Cord Compression

Early – Head Compression

Accelerations – Okay

Late – Placental Insufficiency

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81
Q

Late decel on FHR monitoring = ?

A

Fetal Heart Rate: mnemonic

VEAL CHOP

Variable – Cord Compression

Early – Head Compression

Accelerations – Okay

Late – Placental Insufficiency

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82
Q

MC condition a/w placental abruption?

A

Maternal hypertension, including essential hypertension, gestational hypertension and preeclampsia.

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83
Q

4 T’s of PPH

A

Uterine ATony - MCC
Trauma to birth canal
ReTention
Coagulopathy or Thrombin d/o

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84
Q

Tx uterine atony

A

Treatment is uterine massage
Oxytocin
Prostaglandins
Surgery

85
Q

Pregnancy category risk A

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
86
Q

Pregnancy category risk B

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
87
Q

Pregnancy category risk C

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
88
Q

Pregnancy category risk D

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
89
Q

Pregnancy category risk X

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
90
Q

PID ROSH Facts

A

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.

91
Q

Classic US appearance of ovarian torsion?

A

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

92
Q

Risk factors for ovarian torsion

A

Ovarian mass (>4-5cm)= MOST important risk factor

Pregnancy
Ovulation induction
Prior torsion

93
Q

Gold standard for ovarian torsion diagnosis?

A

Laparoscopy

94
Q

What is the generic of Nexplanon implant?

A

Etonogestrol

95
Q

Uterine fibroids are most common in which race?

A

African americans = MUCH more common - aka if given an african american patient with heavy vaginal bleeding, pick a uterine fibroid/leiomyoma!!!

96
Q

What hormone abnormalities do you find in PCOS?

A

HIGH LH!!!

(2/2 abnormal GnRH pulsation release)

Think PCOS = 4 divided by 2 = LH

Serum androgens also elevated

97
Q

Preferred treatment for trichomonas?

A

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

98
Q

Outpatient management PID

A

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.

99
Q

Cervical cancer screening women ages 21-29

A

Cytology alone every three years

100
Q

Cervical cancer screening women aged 30-65

A

Cytology AND
HPV testing every 5 years

DO NOT just do HPV testing alone - need BOTH > 35 YO

101
Q

What is the standard treatment for most breast cancers?

A

Breast-conserving therapy (lumpectomy) w/ sentinal lymph node biopsy

Followed by radiation therapy

+/- more adjuvant therapy depending on tumor and patient characteristics

102
Q

RF Placental abruption

A

MCC HYPERTENSION

Other: Maternal trauma, smoking, prior placental abruption

103
Q

Most classic finding placental abruption on ultrasound & other common findings

A

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)

104
Q

Complications of placental abruption

A

Placental or uterine insufficiency leading to late decelerations, fetal demise, maternal coagulopathy (DIC) and hemorrhagic shock

105
Q

Endometritis treatment

A

POLYMICROBIAL = BROAD SPECTRUM

ADMIT & GIVE IV CLINDA & GENTAMYCIN

106
Q

Hydatidiform mold is a/w which cancer?

A

Choriocarcinoma

107
Q

Classic US finding hydatidiform mole?

A

“Bag of grapes”

“Snowstorm” appearance””

Uterine size > GA

108
Q

CP Hydatidiform mole (gestational trophoblastic disease)

A 
Vaginal bleeding
Pelvic pressure/pain
Uterine size > GA
Hyperemesis gravidarum
Preeclampsia < 20 wks gestation
HTN < 20 wks gestation
109
Q

Pathophys Hydatidiform mole (gestational trophoblastic disease)

A

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

110
Q

RF molar pregnancy

A

Extremes of maternal age

History of previous mole

111
Q

What is serum alpha fetoprotein used as a marker of?

A

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

112
Q

Is the risk of gestational trophoblastic neoplasia higher after a complete mole or a partial mole?

A

Complete mole

113
Q

Treatment hydatidiform mole?

A

Suction D&C

Can also monitor serial quantitative b-hcg to make sure returns to undetectable levels

114
Q

What is the most common form of breast cancer?

A

Infiltrating ductal carcinoma (70-80%)

Also the most common breast cancer among men

115
Q

Which kind of breast cancer is more common in women with BRCA1 mutation?

A

Medullary carcinoma

More common in women w/ BRCA1 and in younger women

116
Q

Screening for breast cancer guidelines - ACOG vs USPSTF?

A

ACOG: Start at 40 YO annually

USPSTF: Start at 50 YO, every 2 years

117
Q

+ HPV infection in 32 YO w/ negative cytology report = next best step?

A

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

118
Q

Options for emergency contraception & when to give

A

Give ASAP but up to 5 days - efficacy decreases

119
Q

What do you do if you miss two or more birth control pills in a pack?

A

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

120
Q

How long do you have to use backup methods (condoms) when starting birth control?

A

On average 7 days for BC to get up & running fully

121
Q

What is the most common benign breast disorder and who does it affect?

A

Fibrocystic breast disease

Women of reproductive age (MC 30-50)

Incidence increases w/ age but hormonally influenced

122
Q

CP fibrocystic breast disease

A

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

123
Q

Diagnosis/workup of fibrocystic breast disease

A

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

124
Q

Fibroadenoma etiology & epidemiology

A

Etiology not clear - E/P may be causative

MC in YOUNG women - age 10-30 YO

125
Q

CP Fibroadenoma (name 5+ characteristics)

A

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

126
Q

Tx fibroadenoma

A

Reassurance & monitoring

Serial breast exam/ mammo

Excision if super painful/uncomfortable

127
Q

Breast mastitis etio, CP, dx, tx

A

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

128
Q

Etiology of nipple discharge

A

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

129
Q

Characteristics of benign nipple discharge vs pathologic

A

Provoked, b/l, multi-ductal

Unilateral unprovoked discharge, uniductal, ANY BLOOD = BAD

130
Q

Labs for nipple discarge

A

Pregnancy test, prolactin levels, thyroid function

131
Q

Hormonal therapy for breast cancer?

A

(ER/PR positive breast CA) =

Tamoxifen (SERM) - 10 yrs

Aromatase inhibitors- 5yrs (anatrazole, aromasin)

132
Q

ADR Tamoxifen

A

DVT, uterine cancer, vasomotor symptoms

133
Q

ADR aromatase inhibitors

A

Less DVT/uterine CA than tamoxifen (SERM) but causes bone loss, myalgias, arthralgias

Contraindicated in pre-menopausal women

134
Q

Which ER/PR positive breast cancer tx is contraindicated in pre-menopausal women?

A

Aromatase inhibitors (anatrazole, exemestane, letrozole)

TAMOXIFEN is what’s given in premnopausal women

135
Q

Are aromatase inhibitors or SERM’s superior therapy for ER/PR positive breast CA patients?

A

Aromatase inhibitors are superior but contraindicated in premenopausal women…

136
Q

MC breast disease 10-30

A

Fibroadenoma

137
Q

MC breast disease 30-50

A

Fibrocystic disease

138
Q

Breast lump > 50 YO

A

Breast CA until proven otherwise

139
Q

Etiology syphilis

A

Treponema pallidium

140
Q

CP Primary syphilis - incubation period?

A

Painless hard chancre (1 month after exposure)

Heals spontaneously after 1-2 months

141
Q

CP Secondary syphilis, when does it occur?

A

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

142
Q

Fitz-Hugh-Curtis syndrome

A

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

143
Q

Latent syphilis definition

A

Asymptomatic disease with serologic proof of infection - further classified as early latent (acquired w/in last year) vs late latent (acquired >1 year ago)

144
Q

CP Tertiary syphilis

A

Occurs YEARS after primary infection

CP = Granulomas of the skin & bones (gummas), cardiovascular lesions (aortic aneurysms), neurosyphilis (tabes dorsalis, paresis, meningovascular disease)

145
Q

Lymphogranuloma venereum etiology

A

C. trachomatis

146
Q

CP neurosyphilis

A

= 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

147
Q

Lymphogranuloma venereum clinical presentation (three stages)

A

Primary lesion: Painless papule on genitals

Secondary stage: Inguinal lymphadenitis, fever, malaise, loss of appetite

Tertiary stage: Rectovaginal fistulas, rectal strictures

148
Q

Lymphogranuloma venereum Diagnosis

A

NAAT, PCR

149
Q

Lymphogranuloma venereum Treatment

A

100mg Doxy BID x 21 days

Think it’s a ton of sylables & it’s the a super long treatment

150
Q

Treatment syphillis

A

Benzathine penicillin G

151
Q

Which disease causes false positive RPR results?

A

Lupus

152
Q

When do you begin suppressive therapy with anti-retrovirals if HSV positive and pregnant?

A

36 weeks

153
Q

Active HSV outbreak in L&D?

A

Deliver via cesarean

154
Q

Chancroid CP

A

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

155
Q

Incubation period chanroid

A

1 week

156
Q

Treatment chancroid

A

AzithrOmycin

Think about how you treat haemophilis influenza w/ z-pak, treat haemophilis ducreyi w/ z-pak as well

+/- Ceftriaxone

157
Q

Etiology chancroid

A

Haemophilus ducreyi

HaemO = ChancrO

158
Q

Clinical Presentation cystocele

A

Feeling fullness, bulge from vagina (worse w/ standing),

159
Q

Baden-walker classification of prolapse - Grade I

A

To the level of the ischial spines

160
Q

Baden-walker classification of prolapse - Grade II

A

Between the ischial spines and the introitus

161
Q

Baden-walker classification of prolapse - Grade III

A

Up to the introitus

162
Q

Baden-walker classification of prolapse - Grade IV

A

Past the introitus

163
Q

Risk factors for prolapse

A

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)

164
Q

Signs/symptoms of prolapse

A 
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

165
Q

Treatment prolapse

A

Asymptomatic - nonsurgical treatment - aka kegels, hormone/estrogen replacement therapy

Symptomatic - tx w/ pessary (especially useful with elderly or when surgery is contraindicated, surgery)

166
Q

Indications for surgery - prolapse

A

When childbearing is completed and/or symptoms are interfering with patient’s functioning and do not respond to nonsurgical treatment

167
Q

Complications of pelvic organ prolapse

A 
Urinary retention
Constipation 
Urinary tract infection 
Ulcerations
Vaginal bleeding
168
Q

Adenomyosis - pathophys

A

Ectopic endoetrial tissue within the myometrium - lining grows backwards into myometrium and causes hypertrophy and hyperplasia of the myoemtrium

169
Q

Adenomyossis - CP

A

HUGE, THICK, “boggy” “globular” uterus

Not well differentiated from surrounding tissue so can’t exise well - why only definitive treatment is hysterectomy

170
Q

Diagnosis adenomyosis

A

Can only be made pathologically

Can coexist with endometriosis and fibroids

171
Q

Risk factors for adenomyosis

A

Parous women
Hx cesarean
Hx D&C

172
Q

Average age of diagnosis adenomyosis

A

40-50 YO

173
Q

Signs/sx adenomyosis

A

Menorrhagia (65%)
Dysmenorrhea (25%)
Chronic pelvic pain

174
Q

Main Ddx for menorrhagia (heavy menstrual bleeding) (old-ish woman)

A

Uterine cancer
Leiomyoma
Adenomyosis
Polyps

175
Q

Diagnosis of adenomyosis

A

Diagnosis only via histology s/p hysterectomy

Transvaginal ultrasound and MRI very helpful - MRI better but more expensive

176
Q

TVUS / MRI “Key words” suspicious for adenomyosis

A

“Asymmetric thickening of myometrium”

“Linear striations” - from stretched tissue

“Loss of clear endo-myometrial border”

“Increased myometrial heterogeneity”

177
Q

Treatment adenomyosis

A

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

178
Q

Endometriosis pathophys & CP

A

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)

179
Q

Types of functional ovarian cyst

A

Follicular cyst
Corpus luteal cyst
Theca lutein cyst
Endometrioma

180
Q

Endometriosis diagnostic tools

A

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

181
Q

Ddx endometriosis

A 
Appendicitis
STD/PID
UTI
Ectopic pregnancy
Primary dysmenorrhea
Ovarian cysts

AKA LOTS OF PAIN

182
Q

Endometriosis complications

A

Endometrioma - “chocolate cyst” - most common on ovaries

Adhesion formation

Pain

Infertility

183
Q

Which GnRH agonist can induce pseudo-menopause to be used as treatment for heavy bleeding, painful periods caused by adenomyosis, endometriosis, fibroids etc?

A

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)

184
Q

Endometriosis tx

A

95% will respond to medical management - OCPs, Lupron etc

If not effective, done w/ child-bearing = hysterectomy with BSO = considered the definitive tx

185
Q

Simple cyst vs complex cyst

A

Simple: Fluid, thin wall (follicular, luteal, cystadenoma)

Complex: Debris, blood, thick wall, septations, hemorrhagic

186
Q

Follicular cyst characteristics

A

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

187
Q

Follicular cyst ultrasound description

A

Simple, unilocular, UNILATERAL, anechoic (black, just fluid in there) cyst w/ thin, smooth wall

188
Q

Corpus luteal cyst - when occur? Thin or thick-walled? simple or complex? Unilateral or bilateral? US description?

A

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

189
Q

Theca lutein cyst - common or rare? Etiology? Unilateral or bilateral? Septations? Vascular?

A

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!

190
Q

Endometrioma - AKA? age group? CP? Monitoring?

A

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

191
Q

PCOS on ultrasound

A

“String of pearls”

> 10 PEIRPHERAL simple cysts

192
Q

Benign ovarian tumors

A

Mature cystic teratoma (dermoid)

Cystadenoma

Cystadenofibroma

193
Q

Complications of cysts and benign tumors

A

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

194
Q

Cystadenoma- serous

A

Benign ovarian tumor
25% are bilateral
PERI-menopausal women

195
Q

Cystadenoma - mucinous

A

Can be very large
Age 20-40 (reproductive)
10% bilateral
Less frequent than serous cystadenoma

196
Q

Cystadenofibroma - common or rare? Benign or malignant? Simple or complex? Age? Treatment?

A

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

197
Q

Si/sx benign ovarian tumors and cysts

A

ASX

Pelvic pain

Fullness, heaviness, pressure, bloating

Irregular bleeding

Sudden/sharp pain –> ruptured cyst

198
Q

Dx ovarian cysts/tumors

A

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

199
Q

Management of cyst based on ultrasound results

Reproductive age
< 5 cm simple cyst

A

Observe

200
Q

Management of cyst based on ultrasound results

Reproductive age
5-7 cm simple cyst

A

US follow up annually - make sure not rapidly enlarging

201
Q

Management of cyst based on ultrasound results

Reproductive age
> 7 cm cyst

A

MRI or surgery for removal

202
Q

Management of cyst based on ultrasound results

Post-menopausal
107 cm cyst

A

Ultrasound annually +/-

CA-125

203
Q

Treatment of ovarian cysts

A

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

204
Q

Endometrioma

A

Initial f/u US in 6-12 weeks
and US annually vs

Cystectomy (see indications)

205
Q

Indications for cystectomy

A

Symptomatic
Persistent 5-10cm cysts
Ovarian torsion
Suspected malignancy

206
Q

Surgery (cystectomy) NOT required with….

A

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

207
Q

Treatment of ovarian cysts

A

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

208
Q

Si/Sx prolapse

A

Fullness/heaviness

NO PAIN

Inability to empty bladder fully, defecatory dysfunction

*PANCE by subspecialty (22 decks)

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