ABNORMAL UTERINE BLEEDING Flashcards
1
Q
menorrhagia
A
many days of bleeding
REGULAR prolonged and heavy bleeding
2
Q
metrorrhagia
A
IRREGULAR bleeding
bleeding BETWEEN PERIODS
3
Q
Menomentrorrhagia
A
REGULAR periods
that are HEAVY & MANY days long
and bleeding BETWEEN periods
4
Q
Oligomenorrhea
A
small amount of flow
OR
long intervals (cycles more than 35 days longs)
5
Q
Polymenorrhea
A
frequent periods , short cycles (less than 21-24 days long)
6
Q
ANOVULATION
A
**very common cause of dysfunctional uterine bleeding (DUB) ***
particularly common at extremes of reproductive year
–> young girl within 1-2 years of menarche (immediately post-menarche)
–>women in perimenopause
7
Q
NORMAL OVULATORY MENSTRUAL CYCLE
A
(1) PROLIFERATIVE phase: follicles making estrogen and causing the endometrium to build up
(2) OVULATION
(3) LUTEAL phase : corpus luteum make progesterone to keep endometrium stable and secretory …corpus luteum degenerates and progesterone drop off….orderly bleeding
8
Q
ANOVULATORY MENSTRUAL CYCLE
A
(1) PROLIFERATIVE phase: follicles making estrogen and causing the endometrium to build up
(2) NO OVULATION !!!
(3) NO CORPUS LUTEUM no progesteron produce to keep endometrium stable and secretory…. no orderly bleeding because there’s no degeneration of corpus luteus to keep things on schedule
9
Q
ANOVULATORY define
A
- high , sustained levels of unopposed estrogen
- *continuously proliferating, fragile endometrium
- *outgrows its blood supply
- *unpredictable sloughing and irregular periods.
seen in :
immediate post menarche because of immature HPO axis it doesn’t yet ovulatory
&
perimenopause women who aren’t ovulatory at all?
10
Q
AMENORRHEA
A
no period for 6 months OR no period for 3 of her normal cycles what to do ??? ---> r/o pregnancy (most common cause of secondary amenorrhea !!) Then...hx and PE finding will guide ....
11
Q
SECONDARY AMENORRHEA
A
**thyroid or pituitary abnormality
check TSH & PROLACTIN LEVEL (can be scary if turn out to be pituitary tumor ) Or it can be medication that elevate prolactin level …
12
Q
What to do with increase PROLACTIN LEVEL?
A
consult
13
Q
Progestogen challenge test
A
**is there adequate estrogen to build up endometrium??
**can the blood get out ??
+ progesterone 7-10 days take= cease withdrawal blood after stop
–> hormonal withdrawal bleed <–
14
Q
Is there adequate estrogen to build up an endometrium?
A
menstrual flow is a reflection of endometrium –presence and amount
estrogen (from the follicles/estrogen factories in the proliferative phase) builds the endometrium thus
- *plenty of estrogen –> endometrium there ->flow
- *minimal/no estrogen–>no endometrium =no flow
15
Q
PCT–> can the blood get out
A
to see a withdraw bleed, the blood must be able to get OUT
OUTFLOW TRACT problems:
16
Q
POLYCYSTIC OVARY SYNDROME (PCOS)
A
(1) ovaries with multiple large follicles
(2) irregular or NO OVULATION
(3) high levels of ANDROGENS
17
Q
OVARIES - in PCOS
A
multiple large follicles :
- -> 12 or more follicle that are 2-9mm in diameter= all try to be dominant
- ->constrast with normal ovary with small follicles competing but only one (dominant) follicle growing large…
18
Q
PCOS & Ovulation
A
IRREGULAR or No Ovulation at all
- *without the orderly development of dominant follicle —> ovulatory dysfunction
- *without orderly ovulation and cyclic rise and fall of estrogen and progesterone= IRREGULAR SPORADIC UNPREDICTABLE MENSES
- *without regular ovulation = infertility can result
19
Q
what happen to a women with undiagnosed PCOS who didn’t have a period for several months?
A
- r/o pregnancy
- check TSH & prolactin
- give her progestogen challenge test –> outflow tract patent? Estrogenized ?
20
Q
PCOS features
A
High levels of androgens
**these are male sex hormones that are usually present in small amounts in women
**androgens source–> ovaries rarely from adrenals
CAUSE: hirsutism (face chin lower abd)
acne (persisting past adolescent
alopecia especially in male pattern
21
Q
type of androgens
A
testosterone, DHEAS, DHEA, 17-OHP
22
Q
insulin resistance
A
very important feature of PCOS
with resulting hyperinsulinemia
often r/t obesity and metabolic syndrome
as with other features of PCOS normal wt women can have PCOS
23
Q
Ovulatory abnormal uterine bleeding (AUB)
A
REGULAR & tend to be cyclic, although bleeding patterns are often abnormal and may include polymenorrhea, oligomenorrhea, midcycle spotting and menorrhagia. MENORRHAGIA is the pattern most frequently observed with ovulatory abnormal bleeding
24
Q
menorrhagia is associate with what pathology ??
A
pelvic pathology –> UTERINE FIBROSIS, ADENOMYOSIS, or endometrial POLYPS
25
systemic cause of AUB ?
- amenorrhea, oligomenorrhea, and menorrhea.
- renal disease, liver disease, thyroid disease, coagulopathies, thrombocytopenia, von Willebrand disease, and coagulation factor deficiencies.
26
Genital Tract etiologies of AUB?
- ->endometrial and cervical cancer often present in the form of metrorrhagia.
- -> infections: chlamydia, gonorrhea, and endometritis may cause irregular spotting d/t irritation and inflammation of the tissues.
- ->fibroids, adenomyosis, and cervical polyps can cause irregular or heavy abnormal uterine bleeding.
- ->leiofibroids cause menorrhagia or menometrorrhagia.
27
outflow tract causes AUB?
usually amenorrhea
| uterine or cervical congenital or structural abnormalities can cause AUB
28
iatrogenic causes of AUB
medications predispose women to AUB include glucocorticoids, tamoxifen, and anticoagulants.
29
Lifestyle causes of AUB
athletic women and anorexic and other eating disorders are at risk for oligomenorrhea and amenorrhea.
30
what are the specifics of medications to treat heavy menstrual bleeding (menorrhagia)
Combined oral Contraceptives (COC's)
progestogen-only therapy
levonorgestrel-releasing IUD (Mirena: LNG-IUS)
31
acute uterine bleeding treatment
estrogen therapy
- -> high dose estrogen stimulates rapid endometrial proliferation and resolves the bleeding from denuded endometrium. Give an antiemetic as well
- replete intravascular volume
- CEE 25mg IV q4-6 hours PRN then CEE 2.5mg-5mg po 4x/day for 2-3 days then add MPA 10mg for 10-14 days (continue CEE)
- COCs 2x-3x/day then taper
32
acute prolonged bleeding treatment
estrogen-progestin therapy
any monophasic COC begin with 1 pill 2x/day decreasing to 1 pill daily.
continue tx for minimum of 2 weeks.
progestin therapy
use only if endometrium is normal or increased in thickness. tx should cont. for 3 weeks decreasing to once daily tx after 7-10 days.
--> medroxyprogesterone acetate 10-20mg 2x/day
OR
--> megestrol 20-40mg 2x/day
OR
--> norethindrone 5mg 2x/day
33
Long-term/chronic management heavy uterine bleeding
cyclic MPA 10mg/day for 10-14 days every 30-40 days
CC (oral, patch, ring)
oral micronized progesterone 300mg for 10-14days every 30-40days
Depot medroxyprogesterone acetate (depo-provera) 150mg IM every 3 mos
Levonorgestrel intrauterine system (LNG-IUS, Mirena) most effective with fibroids
NSAIDs-useful for ovulatory idiopathic menorraghia, mechanism of action poorly understood. Thought to block production of prostaglandins increasing platelet aggregation
34
Gonadotropin- Releasing hormone agonists
such as leuprolide acetate (Lupon) nafarelin acetate (Synaarel) and goserelin acetate (Zoladex)
- may be used for a short time period while awaiting to have surgical treatment for heavy bleeding
- not recommended for long term because of side effects r/t estrogen deficiency (hot flashes, bone density, night sweat, ect.)
- expensive but very effective in stopping the bleeding so hemoglobin can rise.
35
Tranexamic Acid (cyklokapron)
an antifibrinolytic agent that reduces menstrual bleeding by 45-60%
2nd line option for women who cannot or do not wish to use hormonal options
it is considered first line treatment for ovulatory AUB and Von Willebrand disease
-contraindicated in women with hx or at risk for thrombosis
dose is 1gm taken 3-4 times daily
s/e are rare but include nausea and leg cramps.
36
what are the special concerns of perimenopausal women with AUB?
--> incidence of AUB increases as the women approaches menopause.
ANOVULATORY cycles represents a continuation of declining ovarian function
-->women should be educated early about health promoting activities that offset risks associated with menopause such as OSTEOPOROSIS
they should be encouraged to exercise regularly and modify their diets to include foods rich in iron and calcium; in addition if they smoke, they should be counseled about quiting.
37
Hypothalamus Pituitary Ovarian (HPO) axis
--> most affected by the normal life-cycle transitions that occur during the first 2 years after menarche & 3 years prior to menopause; thus irregular bleeding during this time may be reflection of normal functioning.
38
anovulatory DUB
--> often seen during these times and it is high, sustained levels of unopposed estrogen, continuously proliferating, fragile endometrium, outgrow it blood supply, unpredictable sloughing and irregular periods. No ovulation and no corpus luteum causes no orderly bleeding.
39
primary amenorrhea
failure to begins menses by age of 16
* age is an important criterion in making the differential dx of primary vs secondary
* primary is usually indicative of HPOaxis disorder of anatomic factors, sucha s OUTFLOW OBSTRUCTION
* PE for primary needs to focus on identifying the maturation of secondary sex characteristic (tanner development and pubic hair pattern) and establishing outflow tract patency "has any vaginal bleeding occured?"
- family hx or anatomic or genetic abnormalities need to be explored.
40
Secondary amenorrhea
cessation of established regular menstruation for 6 months or longer
41
Progestin challenge test provide what information ?
(1) is the adequate estrogen to build up the endometrium?
-->menstrual flow is a reflection of the endometrium-presence and amount
--> estrogen (from the follicles/estrogen factories in the proliferative phase) builds the endometrium ... thus : plenty of estrogen=endometrium there->flow
minimal/no estrogen=no endometrium-> no flow
(2) can the blood get out?
42
What conditions that would cause a woman to be amenorrheic and then have positive or negative progestin challenge test?
POSITIVE -> amenorrhea is d/t anovulation
NEGATIVE -> or no bleeding after progesterone withdrawal then the patient's amenorrhea is likely d/t (a) low serum estradiol
(b) HPO axis dysfunction
(c) nonreactive endometrium
(d) problem with uterine outflow tract, such as CERVICAL STENOSIS or UTERINE SYNECHIAE (asherman's syndrome)
43
distinguish between HYPOESTROGENISM or uterine outflow tract problem/nonreactive endometrium
estrogen may be administered followed by a course of progestin in order to induce withdrawal bleeding. if the patient experiences withdrawal bleeding with the combined estrogen/progestin therapy, then amenorrhea is likely due to low estrogen.
44
Hyper-androgenic disorders
PCOS are predominantly --> ANOVULATORY and they typically maintain relatively steady levels of gonadotropins and sex steroids instead of experiencing the fluctuation in these levels characteristic of normal menstrual cycle.
* *Serum LH are HIGHER than normal ovulate women
* *relatively constant LH pulse frequency of approx. one pulse per hours, whereas ovulatory women have cyclic variation in LH frequency
* *this increased LH frequency is caused by GnRH pulse frequency which also causes FSH levels to be at the low end of the normal range.
* * FSH levels are also decreased because of increased estrone levels resulting from peripheral conversion of increased androstendione
* *increased androgen production seen in PCOS occurs in the ovaries as result of increased LH stimulation
* *without the orderly development of a dominant follicle --->ovulation dysfunction
* *without orderly ovulation and cyclic rise and fall of estrogen and progesterone--IRREGULAR SPORADIC UNPREDICTABLE MENSES
* *without regular ovulation -->INFERTILITY result
45
diagnostic test for PCOS
```
serum prolactin
TSH
fasting lipid profile
2 hours glucose tolerate test
serum progesterone
androgen level
17-hydroxyprogesterone
U/S pelvic to assess polycystic ovaries and identify endometrial hyperplasia.
```
46
17-hydroxyprogesterone
test performed to asses for non-classical or late onset congenital adrenal hyperplasia, which is characterized by excessive adrenal androgen production and can present very similary to PCOS
47
management of PCOS
improving clinical signs of hyperandrogenism, regulating menstrual cycles
protecting the endometrium
preventing long-term sequelae of PCOS
```
COCs
progestogens
antiandrogens,
insulin sensitizing agents
topical preparation (Vaniqa) for facial hirsutism, GnRH
```
48
diagnose PCOs
Rottardam PCOS consensus group (2/3 must be present to make PCOS diagnosis
(1) oligo or anovulation
(2) clinical and/or biochemical signs of hyperandrogenism
(3) polycystic ovaries
49
why does dysmenorrhea happen? what hormones or processes are involved?
--> increase endometrial PROSTAGLANDIN production associated with pain.
increase or imbalance in the quantity of prostaglandin present in menstrual fluids occurs.
Excessive amount of prostaglandins cause the uterus to contract abnormally and reduce uterine blood flow and oxygenation, giving rise to pain
prostaglandin release>uterine contractions> decreased uterine blood flow> uterine hypoxia>pain
50
what are the standard treatments for dysmenorrhea ?
--> no diagnostics for primary dysmenorrhea
NSAIDs combined hormonal contraceptive are mainstay of pharmacologic management
51
How would you assess a woman with PMS symptoms?
- symptoms beginning at or soon after ovulation, with escalation in the LUTEAL phase
- worst symptoms in week preceding (before) menses.
- symptoms gone or much better at onset of menses and for first two weeks of new cycle
PE & dx: none is specific to PMS
only those needed to rule out other causes
52
PMS management
--lifestyle approaches: exercise, reduce caffeine, sodium and alcohol, and increase complex CHO
-- supplements/herbs : calcium magnesium, chasteberry
--physical symptoms --> OCPs NSAIDs
--> mood symptoms: SSRIs
luteal phase or beginning with symptoms dosing are often great option
response often seen in first cycle of use
choose a long half-life SSRI if using therapy intermittently
**Fluoxetine (prozac)
**sertraline (Zoloft)
53
Endometrial cancers
post menopausal women
50-60 y.o POSTMENOPAUSAL : any bleeding is abnormal and should be evaluated.
90% present with abnormal uterine bleeding
**in MENSTRUATING WOMEN: this symptom can take the form of bleeding between periods of excessive, prolonged menstrual flow
54
risk factor of endometrial cancers
estrogen therapy >5 years, taking tamoxifen, early menarche, late menopause, hx infertility or nulliparity, obesity, chronic anovulation, DM, high fat diet, ovarian CA, hereditary
55
Ovarian cancer
most are diagnosed when the disease has reached an advanced stage.
symptoms are vague & offer only subtle signs of its presence, such as abdominal bloating, discomfort, dyspepsia, fatigue, back pain, change in bowel or bladder, urinary incontinence, unexplained wt. loss or gain.
advanced signs are anorexia, n/v ascites, abdominal or back pain, an abdominal mass, or pleural effusion.
56
risk factor for ovarian cancer
family hx
BRCA 1 or 2 genetic mutation
increase with age nulliparity prolong estrogen therapy in postmenopausal women, use of fertility drugs.
57
Endometrial biopsy
office procedure accepted as the first step in dx ENDOMETRIAL CA in pt with postmenopausal bleeding.
biopsy is obtained through the use of endometrial suction catheter that is inserted through the cervix into the uterine cavity.
these biopsies detect 80-90% of endometrial CA if an adequate tissue sample is obtained.
if biopsy result fails to provide sufficient diagnostic info or if abnormal bleeding persists, a D&C with or without hysteroscopy is recommended.
58
pelvic U/S
used as an adjunctive means of evaluation for endometrial hyperplasia as well as polyps myomas and structural abnormalities of the uterus. An endometrial thickness of greater than 5mm in a menopausal women is considered an indication for further evaluation
59
Saline infusion sonohysterography
refers to a procedure in which fluid is instilled into uterine cavity transcervically to provide enhance endometrial visualization during transvaginal ultrasound examination.
the technique improves sonographic detection of endometrial pathology, such as polyps, hyperplasia, cancer, leiomyomas, and adhesions. in addition, it can help avoid invasive dx procedures in some pts. as well as optimize the preoperative triage process for those women who require therapeutic intervention. it is easily and rapidly performed at minimal cost, well-tolerated by pts. and is virtually devoid of complications.
60
vulvar skin changes
diagnose --> biopsy
61
cervical polyps
diagnose--> speculum exam, moist, red & glandular, arise from a stalk in cervical canal
62
Nabothian cysts
diagnose--> physical exam
63
ovarian cysts
diagnose--> transvaginal U/S
64
adenomyosis
diagnose--> U/S 83-85% MRI, definitive diagnosis with hysterectomy
65
endometriosis
diagnose--> laparoscopy with biopsy is gold standard
adolescents: CC are first line treatment
(lack of treatment can pose a more severe risk of future fertility)
infertility: age duration of infertility, family hx, pelvic pain, and stage of endometriosis should be taken into account when developing management plan. in vitro may be needed.
66
uterine fibroids
diagnose --> U/S
pregnant women-growth remains stable during pregnancy and postpartum rapid estrogen loss and vasculature reduction can lead to fibroid degeneration with attendant bleeding and pain. Fibroid complications during pregnancy include preterm, spontaneous AB, abruption, pp hemorrhage.
Older women: decrease hormone in menopause often leads in reduction of uterine fibroid size
cultures: bleeding during sex may be taboo or loss of reproductive capability
67
Pelvic pain
diagnose--> CT, MRI, laparoscopy
68
what conditions are likely to be asymptomatic?
vulvar skin changes
cervical polyps
nabothian cysts
fibroids
69
Ovarian masses
adolescent: functional cysts both follicular and luteal are common.
premature HPO axis allows for more anovulatory cycles, leading to more persistent simply cysts. early evidence of PCOS may manifest in this age group
pregnant women: more ovarian masses are being dx early pregnancy owing to the increasing use of 1st trimester U/S. Corpus luteum cyst and mature cystic teratomas are more common reported adenexal masses during pregnancy.
risk of malignancy and acute complications during pregnancy is low
older women-postmenopausal women have an increased incidence of ovarian CA, and benign functional cysts are rare in this age group. therefore, an ovarian mass in a post-menopausal women should be considered highly suspicious for malignancy and thoroughly evaluated.
