Menstrual and Uterine disorders Flashcards

1
Q

what 3 processes do we need to have normal menses?

A
  1. intact HPO axis
  2. endometrium responsive to hormal stimulation
  3. intact outflow tract from internal to external genitalia
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2
Q

what is Primary Amenorrhea

A

Absence of menses…

  • By age 13 (if sexual development also impaired)
  • By age 15 (if normal sexual development)
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3
Q

MCC of primary amenorrhea? other causes?

A

genetic or anatomic abnormality

  1. 50% - abnml chromosomes → gonadal dysgenesis - ovarian insufficiency due to premature depletion of oocytes
  2. 20% - Hypothalamic hypogonadism
  3. Other:
    - GU - absent genitalia; transverse vaginal septum; imperforate hymen
    - Endo - pituitary disease; androgen insensitivity
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4
Q

definition of Secondary Amenorrhea

A

Absence of menses for >3 cycles or 6 consecutive months in a previously menstruating pt

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5
Q

MCC of secondary amenorrhea?
other causes?

A
  1. pregnancy
  2. Other common causes - galactorrhea, PCOS, hypothalamic or pituitary disease, adrenal hyperplasia
  3. Less common - premature ovarian failure, drug-induced
  4. Rare - Other endocrine disease (DM, thyroid, adrenal), cirrhosis, renal failure, malnutrition
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6
Q

3 main categories of causes of amenorrhea?

A
  1. Hypothalamic-Pituitary Dysfunction
  2. Ovarian causes
  3. Anatomic Causes
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7
Q

what can cause Hypothalamic-Pituitary Dysfunction that ultimately causes amenorrhea?

A
  1. GnRH deficiency
  2. Pituitary dysfunction
    - Hyperprolactinemia
    - Sheehan’s syndrome - postpartum
    pituitary necrosis due to hypovolemia
  3. Surgical destruction
  4. Infiltrative diseases
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8
Q

ovarian causes that causes amenorrhea

A
  1. Gonadal dysgenesis
  2. Ovarian failure
  3. Abnormal steroid enzymes - Unable to produce hormones
  4. Ovarian resistance - Follicles do not respond to gonadotropins
  5. Polycystic Ovarian Syndrome (PCOS)
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9
Q

3 types of ovarian failure?

A
  • Primary - directly due to ovaries
  • Secondary - due to hypothalamic or pituitary disease
  • Premature - onset of menopause in women <40 y/o
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10
Q

anatomic causes that causes amenorrhea?

A
  1. Mullerian Dysgenesis - congenital absence of uterus and upper ⅔ of vagina; May ovulate and have normal secondary sex characteristics
  2. Vaginal agenesis
  3. Transverse vaginal septum
  4. Imperforate hymen
  5. Asherman’s syndrome - uterine synechiae (adhesions); Often due to dilation and curettage
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11
Q

w/u for primary amenorrhea if (+) 2o sex characteristics

A
  1. Evaluate anatomy → PE, US; check karyotype
  2. Pregnancy test

Ovaries are producing estrogen

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12
Q

w/u for primary amenorrhea if (-) 2o sex characteristics

A
  1. Evaluate anatomy
  2. Check prolactin and TSH
  3. Check LH and FSH
    - Low → hypothalamic/pituitary disease, stress, low weight/malnutrition = MRI
    - High → ovarian failure = Check karyotype

Ovaries aren’t producing estrogen

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13
Q

w/u for secondary amenorrhea

A
  1. Physical exam +/- imaging
  2. Pregnancy test
  3. TSH and Prolactin
    - If abnormal TSH → thyroid disease
    - If abnormal prolactin → pituitary imaging
  4. Progesterone Challenge Test
    - If bleeding occurs, endometrium is intact but progesterone is lacking
    - Anovulation - no production of progesterone by corpus luteum
  5. Estrogen + Progesterone Challenge Test
    - No bleed → unresponsive endometrium or blockage of outflow
    - If bleeding occurs, suspect hypogonadism
  6. FSH and LH
    - If high → primary/premature ovarian failure
    - If low → secondary ovarian failure
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14
Q

complications of amenorrhea

A
  1. Infertility
  2. Lack of normal physical sexual development
  3. Osteoporosis and fractures
  4. Endometrial hyperplasia and carcinoma
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15
Q

tx for amenorrhea

A
  1. Correction of underlying disease
  2. If desiring pregnancy - ovulation induction
    - Letrozole (Femara), clomiphene (Clomid)
    - Less common - dopamine agonist, gonadotropins
  3. If not desiring pregnancy - estrogen/ progesterone
    - Maintain bone density, reduce genital atrophy or other menopausal s/s
    - Many women do well on COC
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16
Q

Painful menstruation that inhibits normal activity and requires medication

A

Dysmenorrhea

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17
Q

3 types of Dysmenorrhea

A
  1. Primary - no organic, demonstrable cause
  2. Secondary - presence of another disorder that could cause s/s (endometriosis, adenomyosis, PID, cervical stenosis, fibroids, endometrial polyps)
  3. Membranous - due to passage of a cast of the endometrium through an undilated cervix (rare)
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18
Q

Dysmenorrhea is associated with _____ activity during ovulatory cycle
Abnormal uterine contractions → dec blood flow to uterus → uterine hypoxia
Leukotrienes also contribute
Psych factors may also be involved

A

prostaglandin

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19
Q

clinical findings of Dysmenorrhea

A

Pain - hallmark characteristic

  1. intermittent intense cramps or dull, continuous ache
  2. at menses or up to 1-2 d prior; Subsides 12-72 hrs after menses begins
  3. MC recurs
  4. lower abdomen and suprapubic region; lower back and/or thighs possible
  5. Impact on ADLs
  6. N/V/D, malaise, and/or HA
  7. No significant pelvic disease on PE - pelvic tenderness possible
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20
Q

tx of dysmenorrhea

A
  • NSAIDs; acetaminophen, consider short-term codeine/opioid if severe
  • Continuous heat to abdomen - as effective as ibuprofen, more than acetaminophen
  • Hormonal Contraceptives - if no relief from NSAIDs
  • Other - Exercise, TENS unit, Ca, Mg
  • refractory - surgery
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21
Q

what is Psychoneuroendocrine disorder

A
  1. Restricted to luteal phase of menstrual cycle
  2. Biologic, psychological, and social parameters
  3. Poorly understood; not associated with pathologic hormone levels - Serotonergic dysfunction and decreased GABA levels found
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22
Q

PMs and PMDD MC at what age?

A

late 20s to early 30s

Up to 75% of women experience

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23
Q

Non-Pharmacologic tx for for mild-moderate PMS/PMDD

A
  1. Change in eating habits
    - Avoid or limit - caffeine, alc, tobacco, chocolate, sodium
    - small freq meals high in complex carbs
  2. Aerobic exercise, stress management and/or CBT
  3. Chasteberry, Calcium carbonate (bloating, food cravings, pain), Mg (water retention), Vitamin B6 and vitamin E
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24
Q

medications for mild-moderate PMS/PMDD

A
  • NSAIDs - headache, breast or abdominopelvic pain
  • Spironolactone - cyclic edema
  • Bromocriptine (dopamine agonist) - breast pain
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25
Q

tx for severe PMS/PMDD

A
  1. SSRIs - first-line
  2. Hormonal contraception - Often use contraceptives with drospirenone ( Yaz, Yasmin, Beyaz)
  3. consider alprazolam
  4. Refractory - GnRH agonists - Can induce “medical menopause”
  5. Definitive - BL oophorectomy +/- hysterectomy
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26
Q

Encompasses both abnormal menstrual bleeding and bleeding due to underlying causes or diseases
Pregnancy, GU disease, systemic disease, cancer

A

Dysfunctional Uterine Bleeding

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27
Q

first eval of DUB

A
  1. bleeding hx
  2. PE
  3. lab test - CBC, hCG, TSH
  4. cervical cytology - can help screen for invasive cervical lesions
    - Endometrial cells in postmenopausal pt - abnormal unless on MHT
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28
Q

further w/u for DUB

A
  1. Pelvic US
    - Transvaginal - empty bladder - pelvic organs
    - Transabdominal - full bladder - less detail, wider visualization
    - Sonohysterography - saline injected in intrauterine cavity - increased sensitivity
  2. Endometrial Bx
  3. D&C
  4. Hysteroscopy - Gold standard for eval pathology in uterine cavity
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29
Q

when can observation be the mgmt for DUB?

A

premenopausal - if serious pathology ruled out and not impacting patient functioning or quality of life

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30
Q

tx for premenopausal DUB

A
  1. observation
  2. hormones - COC, estrogen
  3. acute hemorrhage - IV estrogen
  4. refractory - levonorgestrel-releasing IUD, D&C (temporary fix) or endometrial ablation
  5. Definitive - hysterectomy
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31
Q

causes for postmenopausal DUB

A
  1. Exogenous hormones - MCC postmenopausal uterine bleed - Menses usually stop 6-12 months after discontinuing MHT
  2. Vaginal Atrophy - MCC lower GU tract postmenopausal bleed
    - lubricants, topical or systemic estrogen; avoidance of trauma
  3. Tumors of Reproductive Tract - surgery possible
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32
Q

Hysteroscopic procedures - destroy or resect endometrium → eumenorrhea
Similar outcomes with bleeding and patient satisfaction between first and second generation procedures

A

Endometrial Ablations

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33
Q

what are the 1st gen Endometrial Ablations

A
  1. Endometrial vaporization (Nd-YAG)
  2. Rollerball electrosurgical desiccation
  3. Endometrial resection (electrosurgery)
  • Direct hysteroscopic guidance
  • Advanced skills and training
  • Longer operating times; More complications
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34
Q

what are the 2nd gen endometrial ablations?

A
  1. Do not require direct hysteroscopic guidance to perform
  2. Quicker and less complicated
  3. Thermal energy
  4. Cryosurgery
  5. Radiofrequency electrosurgery
  6. Microwave
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35
Q

MC sign from endometrial ablations?

A
  • Decreased menstrual flow - 70-80% of patients
  • Amenorrhea - 15-35%
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36
Q

endometrial ablations are CI if patients want what?
What happens if the CI happens?

A
  • who desire future fertility
  • Patient will still need adequate post-op contraception
  • If pregnancy occurs - miscarriage, prematurity, abnormal placentation, perinatal ablation
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37
Q

T/F: patients need to be treated prophylactically with abx for endometrial ablation

A

F: not needed MC

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38
Q

pts may premedicate for 1-2 mo with tx that cause endometrial atrophy, what are they?

A
  • GnRH agonist, combination oral contraceptives, progestins
  • Alternatively may consider curettage before procedure
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39
Q

CIs for endometrial ablations

A
  1. Obstetric - Pregnancy, Women wishing to preserve fertility
  2. Endometrial hyperplasia or genital tract cancer
  3. Postmenopausal women
  4. Acute pelvic infection
  5. Expectation of amenorrhea
  6. IUD in place
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40
Q

concerns if endometrial ablation is done

not CIs

A
  1. Patients at high risk for endometrial cancer
  2. Large or distorted endometrial cavity
  3. Prior uterine surgery
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41
Q
  1. First tool for endometrial ablation
  2. Uterus is distended with saline
  3. laser fiber touches endometrium and is dragged across endometrial surface - Creates 5-6mm deep furrows in endometrium
A

Vaporization (Nd-YAG Laser) - 1st gen

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42
Q

2-4 mm ball or barrel shaped electrode
Shorter operating time, less perforation than other first gen methods
Does not work for intracavitary lesions

A

Rollerball Ablation - 1st gen

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43
Q
  1. Less expensive and larger loop diameter than laser ablation
  2. Resectoscope with electrical current used to excise strips of endometrium
  3. Higher rates of perforation
A

Endometrial Resection - 1st gen

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44
Q
  1. Uncontained saline solution heated and recirculated for 10 minutes
    - Low pressure to avoid opening fallopian tubes to peritoneal cavity
    - Water seal to avoid leakage into vagina
  2. Allows direct observation of endometrium as it is being destroyed
  3. Higher burn risk than other 2nd-gen methods
  4. Can use with anatomically abnormal uterus
A

Hysteroscopic Thermal Ablation - 2nd gen

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45
Q
  1. Fan-shaped mesh device contours to shape of endometrial cavity
    - Uses suction to improve contact with mesh and remove vapor
    - Radiofrequency run through mesh fan to desiccate endometrium
  2. Does not require endometrial preparation
  3. Has been used in patients with small submucosal leiomyomas and polyps
A

Radiofrequency Thermal Ablation - 2nd gen

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46
Q
  1. Silicone device contours to shape of endometrial cavity
    - Filled with RF-heated argon gas
    - Liquid produced during procedure is also heated, providing hot liquid thermal ablation
  2. Does not require endometrial preparation
  3. Has not been studied in patients with fibroids
  4. Higher rates of normal or no menstrual flow after the procedure
A

Thermal + RF Thermal Ablation - 2nd gen

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47
Q
  1. Uterus is sealed off with balloons
    - Uterine cavity then filled with high-temperature water vapor
    - Thermal injury causes scarring to endometrium
  2. Does not require endometrial preparation
  3. May be used in patients with irregular uterine cavity contour
A

Water Vapor Thermal Ablation - 2nd gen

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48
Q
  1. Generates temperatures -100 to -120 C to produce an iceball in the endometrial cavity
  2. Endometrium undergoes cryonecrosis due to low temperatures
  3. Less pain than thermal energy procedures
A

Cryoablation - 2nd gen

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49
Q

what are the 2 endometrial ablation that are no longer in the US?

A
  1. Thermal Balloon Ablation
  2. Microwave Ablation
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50
Q

Aberrant growth of endometrium outside uterine cavity
Most common GYN diagnosis responsible for hospitalization in women 15-44

A

Endometriosis

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51
Q

Endometriosis MC in who?

A
  1. 53% of adolescents with severe pelvic pain warranting surgical evaluation
  2. 25-35% of infertile women
  3. 6-10% of women in reproductive age group
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52
Q

possible causes of endometriosis

A
  1. Retrograde menstruation
  2. Genetic predisposition
  3. Altered immunity → inhibited ability to recognize abnormal endometrial implants
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53
Q

common implant sites of endometriosis

A
  1. ovary, uterine cul-de-sac, pelvic ligaments, uterus, fallopian tubes, large intestine
  2. Other sites - small bowel, bladder, ureters, vagina, cervix, scars, umbilicus
  3. Distant sites - rare - lung, brain, kidney
54
Q

RF for endometriosis

A
  1. (+) Family history
  2. Early menarche
  3. Nulliparity
  4. Long duration of flow
  5. Heavy menstrual bleeding
  6. Shorter menstrual cycles
55
Q

negative risk factors of endometriosis

A
  1. Regular exercise
  2. Late menarche
  3. Higher parity
  4. Longer duration of lactation
56
Q

s/s of endomentriosis

A
  1. dysmenorrhea (79%), pelvic pain (69%) dyspareunia (45%), infertility (26%)
  2. Severity does not correlate with extent of lesions
  3. May be asx or only present with infertility!
  4. constant pelvic pain or sacral backache
    - Often worse just before menses, may persist through menses
    - May be accompanied by pelvic pressure
57
Q

other sx of endometriosis based on the sites?

A
  • Urinary - hematuria, irritative voiding
  • Bowel - bloody stool, diarrhea, constipation, cramping
  • Menstrual - in addition to dysmenorrhea, premenstrual spotting is possible
58
Q
  1. tender nodules in posterior vaginal fornix or uterosacral ligaments, and pain with uterine motion
    - Uterus may be fixed and retroverted (cul-de-sac adhesions)
    - Tender adnexal masses may be felt
    - Endometrial implants may be found in healed wounds, in the vaginal fornix, or on the cervix
    - MC no findings on PE

dx?

A

endometriosis

59
Q

imaging for endometriosis

A

limited use

  1. TVUS - modality of choice to detect for rectum or rectovaginal septum
  2. MRI - may help diagnose equivocal cases
60
Q

definitive dx for endometriosis and findings?

A

surgery (laparoscopy) with bx

  • Early lesions - small, red, petechial
  • Larger - cystic, dark brown, dark blue or black appearance
  • Surrounding peritoneum - thickened and scarred - “powder burn
  • On ovary- enlarge to several centimeters - “chocolate cysts
61
Q

tx for min-mild sx of endometriosis

A
  1. Expectant management
  2. Analgesics - NSAIDs
  3. Hormonal Tx - combination or progestin-only contraceptives - dec dysmenorrhea and may slow progression
62
Q

tx for Moderate to severe symptoms (unresponsive to mild/mod tx) of endometriosis

A
  1. Hormonal Tx - GnRH agonists or antagonists, danazol, aromatase inhibitors
  2. Neuropathic Pain - gabapentin, pregabalin, TCAs
  3. Surgical - attempt to excise or destroy endometriotic implants
    - Can be done at time of diagnostic laparoscopy
    - Post-op pregnancy rates - depend on severity: 75% (mild), 50-60% (moderate), 30-40% (severe)
63
Q

testosterone derivative; acts like progestin
Inhibits gonadotropin release and enzymes that produce estrogen

what drug?
what SE?

A
  • Danazol
  • oily skin, acne, deepened voice, weight gain, edema, dyslipidemia
64
Q

inhibit enzymes that make estrogens
Can be used as adjuvant treatment to agents such as GnRH agonists

what med?

A

Aromatase Inhibitors - Anastrozole or letrozole

65
Q

SE of GnRH agonists & GnRH antagonists

A

lower BMD, vasomotor symptoms, vaginal dryness, mood changes

66
Q

Infection of upper genital tract
Any combination of - endometritis, salpingitis, tubo-ovarian abscess, pelvic peritonitis

A

Pelvic Inflammatory Disease

67
Q

cause of PID?

pathogens

A
  • Often polymicrobial
  • Associated with gonorrhea and chlamydia
  • May be caused by anaerobes, H. flu, G- rods, streptococci
68
Q

what pts are at highest risk for PID?

A

young, nulliparous, sexually active women with multiple partners

69
Q

PID is the leading cause for ?
how to prevent?

A
  • infertility, ectopic pregnancy
  • Use of barrier contraception
70
Q

lower abdominal pain (insidious or acute)

  • May begin during or just after menses
  • May be worse with coitus, jarring movement
  • bilateral; rarely >2 wks duration
  • RUQ pain - associated perihepatitis (Fitz-Hugh-Curtis syndrome)
  • Other sx - abnml menses, cervical/vaginal discharge, irritative voiding, F, chills, N/V

cervical motion tenderness (“Chandelier sign”)
> 38.3 C (101 F)
BL lower quadrant abd tenderness
inflammation of Skene or Bartholin glands

A

PID

71
Q

w/u for PID

A
  • Pregnancy test - negative
  • Vaginal - WBC in vaginal fluid; + G/C nucleic acid probe
  • CBC - leukocytosis and left shift
  • Inflammatory markers - ESR, CRP may be elevated
  • Imaging - TVUS
  • Laparoscopy
72
Q

TVUS findings that suggest PID?

A
  1. Thickened, fluid-filled fallopian tubes
  2. Free pelvic fluid
  3. Tubo-ovarian complex
  4. Tubal hyperemia
73
Q

dx PID and treat empirically in sexually active young women and at-risk women if:

A
  1. Pelvic or lower abdominal pain with no other cause identified
  2. One or more - cervical motion tenderness, uterine tenderness, adnexal tenderness
74
Q

tx for PID

A

Empiric, broad-spectrum abx for gonorrhea/chlamydia - ceftriaxone + doxy + metronidazole

75
Q

when to admit PID?

A
  1. Complicated - Severe illness, N/V, or high F; Pregnancy; Pelvic abscess (including tubo-ovarian abscess)
  2. Unable to exclude surgical emergency
  3. Failure to respond to, tolerate, or comply with outpt oral tx
76
Q
  • Presentation varies from asx adnexal mass to acute abdomen
  • pelvic and abd pain, fever, N/V
  • severe abdominal tenderness and guarding
  • Pressure can cause rupture of abscess and peritonitis - acute abdomen, septic shock
A

Tubo-Ovarian Abscess

77
Q

classic pt for Tubo-Ovarian Abscess

A

young, low-parity, hx of pelvic infection

78
Q

imaging of choice for tubo-ovarian abscess

A
  • US - Complex, multiloculated adnexal mass
  • CT will also diagnose
79
Q

complications of tubo-ovarian abscess?

A
  1. Unruptured - rupture (15%), sepsis (10-20%); Long-term - reinfection, bowel obstruction, infertility, ectopic pregnancy
  2. Ruptured - septic shock, intra-abdominal abscess, septic emboli
80
Q

tx for tubo-ovarian abscess

A
  1. Unruptured - similar to inpt PID but duration usually 4-6 weeks; surgical drainage if large or no improvement w/ abx
  2. Ruptured - life-threatening emergency; TAH and BSO w/ fluids and abx
  3. TOA in postmenopausal pt - high risk of concurrent malignancy
81
Q

types of pelvic organ prolapse

A
  1. Cystocele - anterior vaginal wall defect (bladder); anterior vaginal prolapse
  2. Uterine prolapse - descent of the uterus
  3. Vaginal vault prolapse - post-hysterectomy
  4. Enterocele - bowel in prolapsed segment of vaginal wall
  5. Rectocele - posterior vaginal wall defect (rectum); posterior vaginal prolapse
82
Q

staging of pelvic organ prolapse

A
  1. Staged based on most severe portion of the prolapse when straining
  2. Pelvic Organ Prolapse Quantification (POP-Q) - most precise and objective
  3. Baden-Walker Halfway System - scores each organ prolapse individually
    - 0 - Normal
    - 1 - halfway to hymen
    - 2 - to hymen
    - 3 - halfway past hymen
    - 4 - Maximum possible descent for site
83
Q

s/s of pelvic organ prolapse

A
  1. Vaginal - fullness, pressure, heaviness, and/or discomfort
    - “Something falling out” or “Sitting on a ball”
    - Soft, reducible mass bulging into vagina or through introitus - inc w/ strain/coughing
    - Coital laxity
  2. Pain - back pain, vaginal pain, and/or pelvic pain
  3. Urinary - stress incontinence, frequency, hesitancy, incomplete bladder emptying; May need to “splint” bladder to void
  4. Defecatory - incomplete emptying, need to strain; May need to “splint” vagina or perineum to defecate
84
Q

RF for pelvic organ prolapse

A
  1. OB/GYN - incr parity, h/o pelvic surgery, Postmenopausal
  2. Age
  3. Obesity or physical debilitation
  4. Chronic coughing (lung disease) or straining (constipation)
  5. Neurologic decline
85
Q

Imaging for pelvic organ prolapse is usually only done if ?

A

other underlying process suspected or equivocal case

86
Q

Physical exam techniques to help dx pelvic organ prolapse

A
  • Inspect vulva and perineum - note prolapse at rest
  • Stress test (cough test) for urinary incontinence
  • Assess strength - vaginal support with strain, anal sphincter tone, pelvic floor strength
  • If no prolapse seen with supine pt, examine in standing position
87
Q

conservative tx options for pelvic organ prolapse

A
  1. Pessary - intravaginal device
  2. Pelvic floor exercises (Kegel Exercises), topical estrogens
88
Q

mgmt of pessary for pelvic organ prolapse?

A
  • Must be fitted by provider - can cause pressure necrosis and ulceration
  • Re-examine 1-2w after pessary placement, 4w after, then q 3-6m or q 2-3m if pt cannot remove and clean device
89
Q

surgical tx for pelvic organ prolapse

A
  • Multiple methods for repair of fibromuscular vaginal wall
  • May involve use of synthetic mesh - Can put at risk for vaginal erosions, dyspareunia, pelvic pain
  • Advise pts - risk for recurrence even after surgical repair
90
Q

Uterine enlargement due to ectopic endometrium deep within the myometrium

A

Adenomyosis

91
Q

cause of Adenomyosis?

A

pregnancy, surgery, dec hormones may weaken myometrium - Allows endometrium to invade

92
Q

RF for adenomyosis

A
  1. Parity - nearly 90% of cases are in parous women
  2. Age - nearly 80% develop in 40s and 50s
93
Q
  1. Menorrhagia, dysmenorrhea
  2. global uterine enlargement
    - Rarely greater than that of a 12 week pregnancy
    - Smooth uterine contour
    - Generalized softening of uterus
    - Minimal hemorrhage during menses
A

Adenomyosis

More areas of invasion = more symptoms

94
Q

w/u for adenomyosis?
findings?

A

TVUS

  • Myometrium - focal thickening, heterogeneous texture, cysts
  • Endometrium - projections into myometrium, ill-defined echo
95
Q

difference between adenomyosis vs leiomyomas on imaging?

A

adenomyosis has poorly defined margins, elliptical shape, lack of calcifications

96
Q

tx options for adenomyosis

A

symptom relief

  1. NSAIDs - pain
  2. COCs, progestin-only contraceptives - pain and bleeding
  3. Endometrial ablation/resection - help somewhat; Will not treat deep lesions
  4. Definitive - hysterectomy
97
Q

adenomyosis sx often subside after what?

A

menopause

98
Q

MC benign neoplasm of female genital tract; Benign smooth muscle tumors
AKA “myomas,” “fibroids,” “fibroid tumors”

A

Leiomyomas

99
Q

3 types of Leiomyomas

A
  1. Submucous - directly beneath endometrial lining
  2. Subserous - directly beneath serosal lining
  3. Intramural - completely within myometrium
100
Q

what two things can leiomyomas do that can become a problem?

A
  1. Can become pedunculated and undergo torsion
  2. Can become parasitic
101
Q
  1. Most are asx
  2. MC - abnormal uterine bleeding, pelvic pressure/pain
    - Pain - if torsion, infarction, degeneration occurs
  3. Local compression of other pelvic organs
  4. Infertility, miscarriage, pregnancy complications
  5. uterus may be enlarged, may have irregular contour
A

Leiomyomas

102
Q

w/u for Leiomyomas

A
  • May see iron-def anemia; Rare - polycythemia d/t myoma EPO production
  • US - confirm presence, and monitor growth
  • MRI - intramural vs submucous
  • Hysterography/Hysteroscopy - confirm cervical or submucous
103
Q

tx for leiomyomas

A
  1. Asx - observation; annual exam
    - No intervention needed unless significant pressure on pelvic organs, severe bleeding/anemia, torsion of pedunculated myoma, or rapid growth
  2. Medical tx - NSAIDs, hormonal therapy (contraceptives, GnRH agonists)
  3. Surgical - myomectomy, hysterectomy, uterine artery embolization; May treat preop w/ hormone tx to reduce myoma size
104
Q

leiomyomas will regress spontaneously after what?

A

menopause

105
Q

MC GYN malignancy

A

Endometrial Cancer

106
Q

Endometrial Cancer MC in who?

A
  1. White - 2.4% lifetime risk; Black - 1.3% lifetime risk; 8% better survival for white women
  2. Peak onset - 70s
    - 20-25% occur in premenopausal women
    - 20-30 yrs possible
107
Q

MCC of endometrial cancer

pathogenesis/physiology

A

MC endometrial hyperplasia

  • Estrogens - stimulate endometrium
  • Progesterones - antiproliferative
  • Long-term estrogen exposure → hyperplasia → cancer
108
Q

MCC of endogenous overproduction of estrogen

A

obesity

109
Q

causes of Abnormally high levels of estrogen in/from?

A
  1. obesity
  2. MetS
  3. PCOS
  4. Exogenous unopposed estrogen therapy
  5. Chronic anovulation
  6. Granulosa cell tumors of ovary
  7. Tamoxifen (SERM) - 2-3x increased risk
110
Q

other RF for endometrial cancer?

A
  1. GYN hx - early menarche, late menopause, low parity
  2. History of breast cancer
  3. Western society - high animal fat in diet
  4. Older age - 75-80% are in postmenopausal women
  5. FHx - Hereditary Nonpolyposis Colorectal Cancer (HPNCC)
  6. Comorbidities including DM, HTN, gallbladder disease
111
Q

what 2 factors reduce risk of endometrial cancer?

A
  1. COC - min 1 yr lasts for 10-20 yrs; Progestin - chemoprotective biologic effect; Progesterone IUDs may also be protective
  2. smoking - less estrogen, wt reduction, earlier menopause, latered hormonal metabolism, current and past smokers
112
Q

MC sx of endometrial hyperplasia?

A

abmml uterine bleeding

113
Q

difference between simple vs complex hyperplasia without atypia

A
  • Simple: 1% progress to endometrial cancer w/o tx; 80% spontaneously regress w/o tx
  • Complex: 3-5% progress to endometrial cancer w/o tx; 85% regress with progestin therapy
114
Q

Endometrial glands lined with enlarged cells
Considered premalignant
Progress to cancer - 10% of simple atypical, 30% of complex atypical

A

Endometrial Hyperplasia with Atypia

115
Q

mgmt for Endometrial Hyperplasia with Atypia

A
  • progestin therapy; Higher rate of relapse after progestin tx than non-atypical lesions
  • If intolerant of progestin therapy or relapse following - hysterectomy
116
Q
  • 85% of cases
  • Younger patients
  • More favorable prognosis
  • Low grade or well-differentiated

which type of endometrial CA?

A

type I

117
Q
  • 15% of cases
  • Older patients
  • Poorer prognosis
  • Independent of estrogen
  • Associated with endometrial atrophy

which type of endometrial CA?

A

Type II Endometrial Cancer

118
Q

classic presentation of endometrial CA?

A

obese, nulliparous, infertile, hypertensive, DM white woman

Only 25% of pts have a known hx of hyperplasia

119
Q

spread of endometrial CA?

A

direct extension, peritoneal implants, lymphatic and/or hematogenous

120
Q

MC type of cancer in endometrial CA?

A

adenocarcinoma

121
Q

which type of endometrial CA is More likely to be in older patients; poorer prognosis
Less associated with hyperestrogenic states

A

Serous

122
Q

which type of endometrial CA is High-grade and aggressive
Not associated with hyperestrogenic state

A

Clear Cell Carcinoma - 1-4%

123
Q

s/s of endometrial CA

A
  • abnml bleeding - MC, earliest sx, Always work-up a postmenopausal pt with bleeding
  • abnml vaginal discharge
  • Lower ab cramps and pain - Cervical os stenosis → hematometra; Can develop abscess and sepsis
  • PE - unremarkable; age-related changes (atrophic vaginitis); +/- Blood; Early - nml uterus, Late - enlarged and/or fixed uterus, local LN and/or ovarian metastases
124
Q

w./u for endometrial CA

A
  1. Pelvic US
    - Endometrial thickness >4 mm in postmenopausal pt - high suspicion, do not defer bx with consistent even if < 4 mm
    - Can be used to monitor asx high-risk pts
  2. Definitive - bx; endometrial biopsy , D&C, hysteroscopy with bx
125
Q

outpatient, minimal or no anesthesia needed
False negative rate - 10%

which type of bx for endometrial CA

A

Endometrial biopsy

If symptomatic and negative bx - need D&C

126
Q

more definitive procedure for diagnosis - larger tissue sample
Done inpatient and under anesthesia
Not curative

which type of bx for endometrial CA

A

D&C

127
Q

other testing for endometrial CA

A
  1. Pap smear
  2. CA-125
  3. CBC
128
Q

tx for endometrial CA

A
  1. Surgery - Total hysterectomy with BL salpingo-oophorectomy and staging with pelvic and periaortic lymphadenectomy
    - Surgery alone may be curative in low-risk, localized disease
  2. Adjuvant - radiation, progesterone, chemo
    - Doxorubicin and cisplatin are 2 most active chemo agents
  3. severe anemia - fluids, blood, uterine tamponade w/ vaginal packing; high-dose radiation if fails.
129
Q

5-year survival rates of each endometrial CA staging?

A
  • Stage I - 80-90%
  • Stage II - 70-80%
  • Stage III - 35-55%
  • Stage IV - 17-22%
130
Q

endometrial CA prognosis worsens with what factors?

A
  1. increasing age
  2. higher pathologic grade
  3. advanced-stage disease
  4. increasing depth of myometrial invasion
  5. lymphovascular invasion