Final Exam Flashcards
Primary Amenorrhea vs Secondary Amenorrhea
Primary- no menarche by age 16
-evaluation if no menarche by 15 or within 3 years of thelarche (breast development); no breast development by age 13
Secondary- lack of menstruation for 3-6 months or the length of 3 menstrual cycles
Amenorrhea Causes
pregnancy
hypothalamic-pituitary dysfunction
ovarian dysfunction
genital outflow alterations
Evaluation for primary amenorrhea
history and physical
lab tests- HCG. FSH, TSH, PRL, possibly LH
Pelvic ultrasound
Primary Amenorrhea evaluation
breast development
presence or absence of uterus
FSH levels
Most important step in amenorrhea workup
determine by physical exam or ultrasonography if there are any anatomic abnormalities of the vagina, cervix, or uterus
elevated FSH level in amenorrhea
probably diagnosis is gonadal dysgenesis
karyotype should be obtained
If the uterus is absent and FSH is normal in amenorrhea
probable diagnosis is Mullerian agenesis or androgen insensitivity syndrome (circulating testosterone is in the male range)
If FSH is normal and breast development is present but imaging detects accumulated blood in uterus (hematometra) or vagina (hematocolpos) in amenorrhea
obstructed outflow tract present
If FSH is low or normal but uterus is present in amenorrhea
workup for degree of pubertal development
distinguish between constitutional delay of puberty and congenital GnRH deficiency
also investigate possible causes of secondary amenorrhea
Initial evaluation for secondary amenorrhea
history and physical
Initial labs: HCG, FSH, TSH, PRL, E2, Total T
If pregnancy test is negative in secondary amenorrhea…
evaluate if the patient has adequate estrogen, a competent endometrium, and a patent outflow tract
do Progesterone Challenge Test
Progesterone Challenge Test
Medroxyprogesterone acetate or micronized progesterone given for 10-14 days and is expected to induce withdrawal bleeding within a week of the test
If bleeding occurs after Progesterone challenge
sufficient estrogen, presumed anovulatory (extra-ovarian sources)
If bleeding does not occur after progesterone challenge
patient may be hypoestrogenic or have an anatomic condition or obstruction
High serum prolactin concentration in secondary amenorrhea
can be increased by stress ore eating
measure at least twice before ordering cranial imaging
screen for thyroid disease- hypothyroidism can cause hyperprolactinemia
refer to endocrinology
High serum FSH concentration in secondary amenorrhea
indicates primary hypogonadism (ovarian failure or insufficiency)
Normal or low serum FSH concentration in secondary amenorrhea
indicates secondary hypogonadism (PCOS or hypothalamic amenorrhea)
High serum androgen concentration in secondary amenorrhea
depending on clinical picture can solidify PCOS diagnosis or may raise question of androgen-secreting tumor of ovary or adrenal gland
refer to endocrinology
Treatment of secondary amenorrhea
directed at correcting the underlying pathology
achieve fertility if desired
prevent complications of the disease process
Treatment of hypothalamic causes of amenorrhea
seen in many athletic women
education on adequate caloric intake and decreased exercise
referrals as appropriate
CBT
management of low bone density
Treatment of hyperprolactinemia in amenorrhea
treatment depends on cause and patient goals
treated by endocrinologist
Treatment of primary ovarian insufficiency in amenorrhea
postmenopausal hormonal therapy for prevention of bone loss
oral contraceptives (intermittent ovarian function)
replacement of estrogen and/or progestin
Treatment of hyperandrogenism in secondary amenorrhea
directed toward achieving women’s goal
relief of hirsutism
resumption of menses
fertility
preventing long-term consequences of PCOS
endometrial hyperplasia
obesity
Abnormal uterine bleeding
majority of cases are just after menarche or perimenopausal period
most cases related pregnancy, structural uterine pathology (fibroids, polyps, adenomyosis)
anovulation
neoplasia
Evaluation of abnormal uterine bleeding
Frequency: normal 24-38 days
Regularity: between cycles, 7-9 days: depending on age
Duration: normal <8 days
Volume: subjective, normal does not interfere with a patients quality of life
Evaluation of AUB
Frequency: normal is 24-38 days
Regularity: between cycles depending on age: 7-9 days
Duration: normal <8 days
Volume: subjective. normal does not interfere with a patient’s quality of life
Most common cause of amenorrhea
pregnancy
Abnormal uterine bleeding causes
failure to ovulate (?)
anovulatory causes- PCOS, obesity, adrenal hyperplasia
Ovulatory causes- typically cyclic; usually anatomic or physical lesion heavy or prolonged bleeding
-fibroids
-adenomyosis
-polyps
-uterine malformation
Chronic estrogen production unopposed by adequate progesterone production
allows for the continued proliferation of the endometrium
thickened endometrium outgrows its blood supply and undergoes focal necrosis with partial shedding
bleeding is usually irregular, prolonged, and heavy
Initial evaluation of AUB
history: medical, gyn/OB, menstrual, sexual, cancer
physical exam
pregnancy test
labs: CBC, cervical Ca screening, STIs
In the first decade after menarche…
HPO axis is immature and may not ovulate each month.. leading to irregular bleeding
Who is most likely to have benign and malignant growths?
women between the age of 40 and menopause
Heavy menstrual bleeding evaluation
Imaging to r/o fibroids, adenomyosis, polyps, malformations
Labs: normal plus ferritin, clotting factors, TSh
Endometrial sampling: hyperplasia or malignancy
Intermenstrual bleeding evaluation
spotting or bleeding throughout month
imaging to r/o polyps scars or defects
Endometrial sampling concern for malignancy
Irregular bleeding evaluation
usually ovulatory dysfunction
imaging to r/o polyps scars or defects
labs: TSH, PRL, Androgens, FSH, E2
Endometrial sampling if symptoms occur >6 months for hyperplasia or malignancy
Treatment of AUB
ensure regular shedding of endometrium and bleeding
use of progesterone for 7-10 days to stimulate withdrawal bleeding
use of COCs to regulate bleeding patterns
endometrial ablation if other treatments are ineffective with no future childbearing
Premenstral syndrome
physical and behavioral symptoms that occur in the second half of menstrual cycle (luteal phase)
abdominal bloating
breast tenderness
HA
edema
anxiety
depression
confusion
social withdrawal
angry outburst
Premenstral dysphoric disorder
affects 3-5% of women outlined in DSM-5 criteria
at least 5 or more symptoms are present in week before menses and resolve in days following menses
distinguish from depression, anxiety, or hypothyroidism
detailed history
if a woman DOES NOT a symptom-free interval they do not have PMS/PMDD
mild to moderate PMS treatment
directed toward specific symptoms
encourage physical acticity
dietary modification- limit caffeine
use of calcium and magnesium supplements
herbal products
therapy, biofeedback, acupuncture, reflexology, relaxation therapy
COC use- continuous use?
PMDD first line treatment
SSRI- fluoxetine, sertraline, paroxetine
if one is not successful, try another!
hormonal therapy
progestin-based contraceptives- DMPA, hormonal IUDs
COCs- continuous use?
Dysmenorrhea
painful menstruation that prevents a woman from doing her normal activities
may be accompanied by diarrhea, nausea, vomiting, headache, and dizziness
primary vs. secondary dysmenorrhea
primary greatest in teens and early 20s- caused by excess prostaglandin F2a produced in the endometrium
secondary becomes more common as a woman ages because of increasing prevalence of causal factors; caused by structural abnormalities or disease processes that occur outside the uterus, within the uterine wall, or within the uterine cavity such as endometriosis adenomyosis, or uterine fibroids
Patient history with dysmenorrhea
heavy menstrual flow with pain- suggestive of adenomyosis, fibroids, polyps
feeling of pelvic heaviness or change in contour of abdomen could be large fibroid or cancer
fever, chills, malaise- signal infection
coexisting complaint of infertility may suggest endometriosis or PID
Primary Dysmenorrhea
caused by excess prostaglandin F2a that is produced in the endometrium; prostaglandin production increases under the influence of progesterone and peaks around menses
can cause uterine contractions with pressures than can exceed 400mmHg
baseline contraction pressure are about 80mmHg, normal baseline is 20mmHg
Prostaglandins
cause muscle contractions and can cause them places other than the uterus, cause N/V/D
Diagnosis of primary dysmenorrhea
recurrent month after months occurring in the first few days of menstruation
dyspareunia generally not found in primary dysmenorrhea
Prostaglandin E2
produced in uterus
potent vasodilator and inhibitor of platelet aggregation (heavy periods)
Secondary dysmenorrhea
caused by structural abnormalities or disease processes outside the uterus, within the uterus, or within uterine wall
endometriosis, tumors, adhesions, PID
pain lasts longer than menstrual period, may start prior to bleeding, become worse during menses, persists after menstruation ends
Clinical features that separate secondary from primary dysmenorrhea
enlarged uterus, pain with intercourse, resistance to effective treatments
Assessment for secondary dysmenorrhea
PE directed toward finding secondary cause
Pelvic- asymmetry or enlargement may suggest tumor or fibroids
Painful nodules in the posterior culdesac with restricted cervical motion may suggest endometriosis
restricted motion may also suggest scaring/inflammation
Obtain cervical cultures- GC and CT, R/O PID
Imaging
laparoscopic exam may establish final diagnosis
Primary dysmenorrhea should not be diagnosed without ruling out…
secondary causes
-PE should be normal in primary
Therapy for dysmenorrhea
vast majority with primary find relief with NSAIDs
heat
exercise
psychotherapy
COC
Reassurance
Therapy for secondary dysmenorrhea
severe cases may require surgical intervention
-pre sacral neurectomy
other procedures targeted toward underlying condition
Acute pelvic pain
lower abdominal or pelvic pain that has lasted less than 3 months
over 1/3 of reproductive aged women will experience non-menstrual pelvic pain
Etiologies of acute pelvic pain
PID
Tube-ovarian abscess
hemorrhage, rupture, or torsion of an ovary or ovarian neoplasm
torsion of fallopian tube
endometriosis
endometritis
dysmenorrhea
ovarian hyperstimulation syndrome
Differential diagnosis for acute pelvic pain
appendicitis
ovarian cyst
pyelonephritis
lower UTI
renal calculi
GI conditions
Acute pelvic pain with positive pregnancy test
r/o ectopic pregnancy or miscarriage
Visceral pain
receptors responsible for these sensations are located on serial surfaces, within the mesentery, and within the walls of hollow viscera
deep, dull, vague, poorly-defined sensation
Visceral pain in acute pelvic pain
distention of a viscous or organ capsule
spasm of intestinal muscularis fibers
inflammation or infection
ischemia from vascular disturbances
hemorrhage
neoplasm
Somatic pain
includes abdominal and pelvic muscle fascia, parietal peritoneum, subcutaneous tissue, and skeletal system
d/t myofascial trigger points
hernia
hematoma
muscle strain or injury
inflammation
trauma
pain directly over inflamed area
pain usually steady and aching in character
tension in area increases pain
will see guarding or rebound tenderness
