Gynecology Flashcards
precocious puberty- age cut-off
before age 8 in girls
before age 9 in boys
does not always have to be treated if not serious or impactful
precocious puberty causes
familial/genetic (nonpathologic)
central (True) precosious puberty: early activation of hypothalamic pituitary- gonadal axis
- image the head
- continuous GnRH analog will suppress LH and FSH
pseudoprecocios puberty: autonomous excess secretion of sex steroids
- image the abdomen
- surgical tumor removal
congenital adrenal hyperplasia
-cortisol replacement
complications:
short stature
social and emotional adjustment issues
precocious puberty isosexual vs heterosexual
iso: premature sexual development appropriate for gender
10% due to CNS lesions/trauma
Complete- all sexual characteristics develop prematurely
incomplete- only 1 sexual characteristic develops prematurely
hetero: virilization of girls (exogenous androgens, androgen- secreting neoplasm, congenital adrenal hyperplasia)
feminization of boys
precocious puberty isosexual vs heterosexual
iso: premature sexual development appropriate for gender
10% due to CNS lesions/trauma
Complete- all sexual characteristics develop prematurely
incomplete- only 1 sexual characteristic develops prematurely
hetero: virilization of girls (exogenous androgens, androgen- secreting neoplasm, congenital adrenal hyperplasia)
feminization of boys
precocious puberty causes
familial/genetic (nonpathologic)
central (True) precosious puberty: early activation of hypothalamic pituitary- gonadal axis
pseudoprecocios puberty: autonomous excess secretion of sex steroids
precocious puberty isosexual vs heterosexual
iso: premature sexual development appropriate for gender
10% due to CNS lesions/trauma
Complete- all sexual characteristics develop prematurely
incomplete- only 1 sexual characteristic develops prematurely
hetero: virilization of girls (exogenous androgens, androgen- secreting neoplasm, congenital adrenal hyperplasia)
feminization of boys
pregesterone
pro-gestation stimulates endometrial development inhibits uterine contraction increases thickness of cervical mucus increases basal body temp inhibits LH and FSH secretion
decrease in progesterone level leads to menstruation (simulate this by giving progesterone and then stopping it)
bHCG
maintains corpus luteum and progesterone secretion
mean age of menarch in the US
13
pregesterone
pro-gestation
True precocious puberty
high LH and FSH
GnRH will increase FSH further
treat by inducing menopause with continuous GnRH analog
mean age of menarch in the US
13
Pseudoprecocios puberty
low LH and FSH
no response when GnRH given
True precocious puberty
high LH and FSH
GnRH will increase FSH further
how long is luteal phase
13-14 days
FSH triggers release of which hormone from follicle?
estradiol
Menopause
end of menstruation due to cessation of ovarian function
Average age: 51.5 years
Premature ovarian failure: amenorrhea for at least 1 year before age 40
Labs, which are not so necessary would show
increased FSH, LH,
decreased estrogen
Menopause is diagnosed with 12 months of amenorrhea in a woman over 45yo (diagnostic and requires no additional work-up)
A woman over age 45 with irregular menses (oligoamenorrhea) and menopausal symptoms (hot flashes, mood changes, sleep disturbances) can be assumed to be going through perimenopause
Serum FSH increases in the perimenopausal period and after menopause, but this is of little diagnostic value beyong obtaining a menstrual history and history of symptoms
If younger than 45, other etiologies for oligo/amenorrhea must be excluded (TSH, serum hCG, prolactin, FSH)
Premature ovarian failure:
amenorrhea for at least 1 year before age 40, or high FSH + menstrual irregularity before age 40
tobacco radiation chemo abdominal disorders pelvic surgery
Perimenopause
ovarian response to FSH and LH decreases
FSH and LH levels increase
Estrogen levels fluctuate
irregular bleeding, sometimes heavier flow
Endometrial biopsy to r/o other causes
Menopause symptoms
hot flashes breast pain sweating fatigue anxiety/depression dyspareunia urinary frequency and dysuria changes in bowel habits vaginal atrophy bladder symptoms stress urinary incontinence
Menopause treatment
Women’s Health Initiative- gave asx post- menopausal women estrogen and progesterone to see if it is cardioprotective, and they had more heart attacks and cardiac events so estrogen is now only used to treat symptoms
Topical estrogen is contraindicated in anyone with history of estrogen- sensitive or breast cancer
Dyspareunia can be treated with
- lubricating agents
- vaginal estrogens
Osteoporosis:
- calcium
- vitamin D
- weight-bearing exercise
- bisphosphonates
- selective estrogen receptor modulators (SERMs)
Hot flashes and mood swings:
-hormone replacement therapy at least for a little while
Pros and cons of hormone replacement therapy for menopause
Pro:
- control of menopause symptoms (hot flashes, vaginal dryness/atrophy, urinary incontinence, emotional lability
- reduced risk of osteoporosis
- reduced risk of colorectal cancer
CONS
- not indicated for prevention of chronic disease, stroke, heart disease, and osteoporosis (USPSTF)
- HRT doubles risk of
- invasive breast cancer (+8 per 10,000) but not noninvasive breast cancer
- endometrial cancer
- venous thromboembolism (+8 PEs per 10,000)
- increases risk of stroke by up to 32-41% (+8 per 10,000)
- increases risk of heart disease by 29% (+7 per 10,000)
- However, if taken at ages 50-59, HRT results in less coronary calcifications on CT scan. This may or may not correlate with less risk of heart disease in women taking HRT during ages 50-59.
- increases risk of biliary disease and need for biliary surgery
Non-hormonal options for treating hot flashes
- Venlafaxine- a good choice if any depression, anxiety, fatigue, isolation. Good first- line drug
- Desvenlafaxine: only non-hormonal drug that is FDA-approved for hot flashes. Also works as an antidepressant
- Clonidine- a good choice if BP control is also needed. SE- dry mouth, constipation, drowsiness
- Gapabentin- good choice if insomnia, restless leg syndrome, seizure d/o, neuropathy, chronic pain
- Time- about 30-50% of women have symptoms improvement within a few months, and most have resolution within 4-5 years
- Placebo: placebo effect is about 20-25% effective in reducing hot flashes
Side effects of estrogen therapy
weight gain nausea breast tenderness headache endometrial proliferation
Side effects of progesterone therapy
acne
depression
hypertension
Primary Amenorrhea
16yo with normal secondary sex characteristics but no menses
13yo with absence of both menses and secondary sex characteristics
Causes of primary amenorrhea
hypothalamic or pituitary dysfunction
anatomic abnormalities
- absent uterus
- vaginal septum
- imperforate hymen
chromosomal abnormalities with gonadal dysgenesis
-Turner syndrome (45XO)
Secondary amenorrhea
absence of menses >6 months in a patient with a prior history of menses
causes: pregnancy premature ovarian failure hypothalamic or pituitary disease acquired uterine abnormalities polycystic ovarian syndrome hyperprolactinemia thyroid disease anorexia nervosa or over-eating
Asherman syndrome
scarring of the uterus that follows infection or postpartum procedure
H and P menstrual history family history medications signs of masculinization -facial hair -voice deepening Tanner stages
Labs to check in amenorrhea
1. beta HCG Thyroid studies (TSH and free T4) Prolactin FSH and LH Androgens -testosterone and DHEA
- progesterone challenge
estrogen-progesterone challenge
progesterone challenge
is the woman producing estrogen and/or having ovulatory cycles?
estrogen stimulates growth of endometrial lining
If a woman doesn’t ovulate then there isn’t a release of progesterone that stabilizes what has grown
After stopping progesterone, there should be menstruation, but only if estrogen was normal and built up the endometrial lining
If progesterone challenge lead to bleeding, consider anovulation to be the explanation for amenorrhea
if progresterone challenge has no effect, then suspect low estrogen levels or outflow tract obstruction to be the causes of amenorrhea
- estrogen-progesterone challenge
estrogen-progesterone challenge
Give estrogen to ensure that the endometrial lining can be present
If the withdrawal of these hormones induces menstruation then you know the patient has a normal outflow tract
What are the basics of a workup of primary amenorrhea
- congenital defects: imperforate hymen, transverse vaginal septum, vaginal agenesis
- if signs of hyperandrogenism, serum testosterone and DHEAS to assess for androgen- secting tumor
- if galactorrhea, then serum prolactin and thyrotropin to assess for prolactinoma
If physical exam shows possible absence of uterus, then obtain a pelvic sonogram
- if uterus absent, then check karyotype and serum testosterone
- androgen insensitivity syndrome (46,XY; elevated testosterone)
- abnormal mullerian development (46, XX; normal female testosterone levels) - If the uterus is present, check beta-HCG and FSH
- if beta-HCG is high- pregnancy
- if FSH low -cranial MRI for hypothalamic or pituitary diseas
- if FSH normal- serum prolactin and thyrotropin
Labs to order for secondary amenorrhea
- serum bHCG to rule out pregnancy
- thorough H and P
- serum prolactin (rule out hyperprolactinemia), serum TSH (rule out thyroid disease), serusm FSH (rule out ovarian failure)
- If signs of hyperandrogenism, then serum DHEAS and total tetosterone
- If all the above are normal or history of dilatation and curettage (D and C), abortion, miscarriage, then progestin withdrawal test (rule out Asherman syndrome)
Treatment for amenorrhea
- modify behavior
- surgical correction
- GnRH or gonadotropin replacement- Leuprolide
- Dopamine agonists
- hormone replacement therapy for symptom management
- Lysis of adhesions and estrogen administration if Asherman syndrome
Primary dysmenorrhea
inflammation/trauma of shedding of endometrial lining
crampy lower abdominal pain n/v HA diarrhea mild tenderness
Secondary dysmenorrhea
Endometriosis PID Fibroids Cysts Adenomyosis
Risk factors for dysmenorrhea
menorrhagia
menarche
dysmenorrhea workup
rule out pregnancy cervical or vaginal cultures urinalysis NSAIDs (less pain and less bleeding if initiated the day before bleeding and continued 16hrs throughout bleeding) hormonal contraception
premenstrual dysphoric disorder (PMDD) and PMS
pain
abnormal mood
autonomic symptoms
in the luteal phase
interferes with daily life characterized by weight gain HA abdominal/pelvic pain abdominal bloating change in bowel habits food cravings mood lability depression fatigue irritability breast tenderness edema abdominal tenderness acne
RF: family history
Tx: NSAIDs, hormonal contraception, exercise, B6, progesterones, SSRIs just during symptoms (5 days per month)
Endometriosis
endometrial tissue outside of the uterus
ovaries broad ligament bowel bladder lungs brain
Theories: retrograde menstruation vascular spread lymphatic spread iatrogenic spread metaplasia
RF:
nulliparity
family history
infertility (50% of cases)
clinical features;
- pelvic pain (most severe during menses, 2-7 days prior to menses and possibly at ovulation)
- 3Ds: dysmenorrhea, deep dyspareunia, and dyschezia (painful defecation during menses), possible blood in stools during menstruation
- infertility
Physical findings:
- localized tenderness in the cul-de-sac or oterosacral ligaments (especially at the time of menses)
- palpable, tender nodules in the cul-de-sac, uterosacral ligaments or rectovaginal septum
- pain with uterine movement
- tender, enlarged adnexal masses especially if there are endometriomas
- Adhesions causing a fixed or retroverted uterus
Labs:
CA-125 increases, not very meaningful though
Biopsy:gunpowder, chocolate
Treatment:
expectant management
pain control with NSAIDs
hormonal therapies: combined OCPs dosed continuously
GnRH agonist given continuously for 6-12 months
Progestin
Danazol
Aromatase inhibitors stop conversion of androgens to estrogens, to decrease stimulation to endometrium
Surgical intervention
laparoscopic surgery
lysing adhesions, addressing infertility, and collecting biopsy specimens in doing so
hysterectomy with bilateral salpingo-oophorectomy (take the ovaries, which secrete much hormone), then proceed with hormone replacement
Adenomyosis
growth of endometrial tissue within uterine wall
painful
The 3 Ds of endometriosis
dysmenorrhea
deep dyspareunia
dyschezia
Common causes of abnormal uterine bleeding
fibroids cancer HPO dysfunction clotting disorders-von Willebrand disease Threatened abortion Molar pregnancy Ectopic pregnancy
PALM-COEIN causes of abnormal uterine bleeding
PALM-COEIN polyp adenomyomas leiomyoma malignancy and hyperplasia coagulopathy ovulatory dysfunction endometrial iatrogenic not yet classified
Workup for abnormal uterine bleeding
H an P:
Ask about the menstrual cycle: how long is it usually?
is it heavy? is it related to intercourse? associated symptoms? family history of bleeding disorder bleeding with medical procedures? contraceptive history rule out GI bleeding and bleeding from the urinary tract
A change in the menstrual cycle clues us into abnormal pathology
Labs: pregnancy test CBC homrones: testosterone, TSH, FSH, LH, prolactin coagulation studies
pap smear
STD testing
endometrial biopsy if >45yo
or if
How long is a menstrual cycle, typically?
21-35 days
polymenorrhea
oligomenorrhea
menstrual cycle >35 days
How long does the period usually last, and how much blood loss is normal?
Generally 3 hrs
seldomly needs to change pads during the night, only passes clots
menorrhagia
Excessive bleeding
Metrorhagia
frequent bleeding
irregular periods- causes
ovulatory dysfunction
anovulatory bleeding is typically heavy, as it occurs only when blood supply to an overgrown endometrium becomes insufficient
regular heavy bleeding suggests fibroid, adenomyosis, or polyp
Bleeding related to intercourse
cervical lesion or polyp
glandular tissue on cervix
MCC AUB
ovulatory dysfunction
AUB and positive bHCG, + intrauterine pregnancy and closed os
threatened abortion
AUB and enlarged uterus + menoetrorrhagia for months
fibroids, molar pregnancy, adenomyosis
AUB and bleeding associated with severe menstrual pelvic pain
endometriosis, adenomyosis
AUB and menorrhagia in a perimenopausal woman
endometrial cancer or hyperplasia
