Chapter 33 Menstrual Disorders Flashcards

1
Q

puberty can start as early as__

A

7 years old

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2
Q

__ hormone is involved in the initiation of puberty

A

leptin hormone

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3
Q

depot medroxyprogesterone acetate leads to reversible bone mineral density loss in adolescents

A

true

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4
Q

meds to improve clinical symptoms of fibroids

A

gonadotropin-releasing hormone ANTAGONISTS, aromatase inhibitors, and antiprogesterone agents

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5
Q

polycystic ovary syndrome is associated with metabolic disorders

A

true

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6
Q

premature ovarian failure (POF) is not equivalent with menopause

A

true

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7
Q

POF associated with

A

cardiovascular disease and endothelial dysfunction

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8
Q

leptin hormone may restore menses in pts with

A

hypothalamic amenorrhea

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9
Q

Normal menstrual cycle

A
early follicular phase
late follicular phase
ovulation
early secretory (luteal phase)
late luteal phase
menstruation
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10
Q

release of negative feedback from __, __, and __ in early follicular phase allows an increase in gonadotropin releasing hormone (GnRH) pulse frequency

A

estradiol
progesterone
inhibin A

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11
Q

FSH rises, recruiting one follicle destined for ovulation

A

true

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12
Q

remainder of __ follicles recruited each month undergo atresia

A

primordial

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13
Q

a follicle is surrounded by 2 types of cells: granulosa and theca cells; FSH receptors in the granulosa cells increase

A

true

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14
Q

aromatization of androgens in granulosa cells begin

A

true

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15
Q

granulosa cells proliferate, and inhibin/activin production (mainly inhibin b) rises

A

true

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16
Q

increased estrogen from dominant follicle leads to proliferation of the endometrium and starts to negatively inhibit FSH secretion

A

true

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17
Q

LATE FOLLICULAR PHASE

LH levels rise , stimulating androgen production in the

A

theca cells

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18
Q

endometrium continues to thicken in the

A

late follicular phase

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19
Q

Ovulation occurs 34-36 hours after onset of LH surge

A

true

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20
Q

LH surge results in the following besides ovulation:

A
  1. resumption of meiosis in the oocyte (not completed until fertilization has occurred)
  2. luteinization of granulosa cells
  3. production of prostaglandins and progesterone within the follicle.
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21
Q

LUTEAL PHASE / early secretory

A

progesterone levels rise rapidly secreted from newly developed corpus luteum.

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22
Q

corpus luteum degenerates __ after ovulation in the absence of HCG

A

9-11 days

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23
Q

abnormal bleeding in adolescents. average age of onset of puberty is

A

9-10 years

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24
Q

sequence of puberty:

A
  1. accelerated growth
  2. breast development
  3. adrenarche
  4. menarche
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25
Q

Menarche occurs within — after thelarche when breast development has reached tanner stage 5

A

2-3 yrs

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26
Q

With sufficient levels of — endometrial lining thickens and first menses occurs

A

Estrogen

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27
Q

By age –, –% of females will have reaches menarche

A

Age 15, 98% reached menarche

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28
Q

Evaluation of irregular menses in adolescents

A

Confirm normal pelvic anatomy with exam and us

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29
Q

Basic lab tests

A

Hcg, tsh, CBC, plt
If menorrhagia is primary complaint, additional labs fibrinogen, prothrombin time, ptt, bleedin time, Bon willebrands factor antigen, rustic erin c cofactor, platelet aggregation studies

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30
Q

Von willebrands most common condition in adolescents

A

13%

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31
Q

Treatment of abnormal bleeding in adolescents

A

Ocp, progestins, depot medroxyprpgesterone acetate,

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32
Q

Adolescents intermenstrual bleeding

A
Pregnancy
Anatomical abnormalities
Anovulation 
Infection 
Malignancy
Hormonal therapy
Chronic systemic diseases
Cervical or vaginal bleeding
33
Q

– is most common complication associated with fibroids secondary to —

A

Postpartum hemorrhage; secondary to decreased uterine contractioity

34
Q

Endometrial polyps incidence rate —

A

10-25%

35
Q

Polyps are rare in women

A

20s

36
Q

Diagnosis of polyp

A

Sis rate of 93%

Hysteroscopy can also used as diagnostic tool and treatment

37
Q

World health organization WHO separates amenorrheic PTs in 3 groups

A

Who 1: no evidence of endogenous estrogen, normal or low fsh, normal prolactin, no evidence of lesion in hypothalamus pituitary region

38
Q

Who 2

A

Evidence of estrogen production, normal prol and fsh

39
Q

Who 3

A

Elevated serum fsh (gonadal failure)

40
Q

Who 1 disorders

A

Most common is hypothalamic amenorrhea. Fsh near normal,high fsh/lh ratio(as seen in prepubertal girls).

41
Q

Causes of hypothalamic amenorrhea:

A

Stress: increase in corticotrophin releasing hormone (Crh) which inhibits gonadotropin secretion

Anorexia and bulimia: changes leptin, neuropeptide y, melanocortins, and Crh lead to low levels o gonadotropin

Excessive exercise: in competitive sports have a 3fold higher risk of hypothalamic amenorrhea

42
Q

Female

Sthle triad

A

Amenorrhe
Abnormal eating
Osteoporosis

43
Q

Hypothalamic amenorrhea causes by low body weight can be reversed

A

Gain weight. Based on higher bmi and lower cortisol level over time

44
Q

Other causes of who1 disorders

A

Kallman syndrome - absence of Gnrh and anosmia

Adrenal hyperplasia - adrenal insufficiency deficient gonadotropin production, and impaired response to gnrh)

45
Q

Who2 disorders

A

Pcos
Clinical or biochemicl evidence of hyperandrogenemia
Ovulating dysfunction
Presence of polycystic ovaries

46
Q

When pcos suspected work up includes

A

Bp, bmi, androgen levels , 17 hydroxyprogesterone ( r/o no classical congenital adrenal hyperplasia), screening for cardio metabolic disorders including fasting lipids and gtt and pelvi us

47
Q

Treatment for anovulation/pcos

A

Restore normal menstrual cycles and normalize bmi through diet and exercise.
Ocps first line treatment in PTs not ttc. Act as anti androgens, estrogen increases sex binding globulins, progesterone suppresses lh which decreases testosterone production, inhibits 5 alpha reductase activity in skin. Regulates
Menses

48
Q

In cases o prolonged heavy bleeding as a result I anovulation any low dose oc can be used

A

Twice a day for at least 5-7 days until bleeding slows followed by one pilldaily

49
Q

Occasionally bleeding is unresponsive to progestins or oc, bleeding might be secondary to a

A

Very thin denuded endometrium rather than a thickened endometrium.

In these cases high dose estrogen can be given:

  1. 25mg conjugated equine estrogens or
  2. 0 mg micronized estradiol every 4-6 hrs x24hrs followed by one pill a day for next 7-10 days
50
Q

Who3 disorder

A

Premature ovarian failure
Turner syndrome
Gonadal dysgenesis
Pituitary

51
Q

Premature ovarian failure

A

Amenorrhea in presence of hypergonadotropic hypogonadism prior to 40
Dx 4 months of amenorrhea and 2menopausal levels of fsh sufficient

52
Q

Premature ovarian failure is distinct from menopause 50% will have resumption of ovarian function after the diagnosis; 5-10% will spontaneously conceive after diagnosis

A

True

53
Q

Turner syndrome

A

45xo
Short stature, web neck, shield chest, renal abnormalities, autoimmune disorders 50% hypothyroidism) cv disorders, hypergonadotropic hypoestrognic amenorrhea
Need echo

54
Q

If uterus is absent on exam what should be ordered

A

MRI, karyotyping , serum testosterone

55
Q

If uterus is present

A

Pregnancy test, fsh, prolactin, tsh

56
Q

Most prolactin adenomyosis successfully treated with

A

Dopamine agonists
Bromocriptine
Cabergoline - fewer side effects and more effective at normalizing prolactin levels

Surgery rarely indicated

57
Q

Women with pig should start hormone therapy replacement to prevent bone loss and cardiovascular complications

A

Low dose estrogen 100ug estradiol patch, 2mg oral micronized estradiol or 1.25mg conjugated equine estradiol

58
Q

Transdermal estradiol often preferred route. It avoids first pass effect on liver
True. If pt has uterus also then what

A

Cyclic progesterone 10mg of medroxyprpgesterone acetate or 200mg of oral micronized progesterone given 12 days each month if uterus is present

59
Q

cylic progesterone therapy 5-10mg of medroxyprogesterone acetate or 200mcg of micronized progetserone how is it used?

A

2 weeks every month will be sufficient for restoring menses and protecting the endometrium if contraception is not desired. in addition to stabilizing endometrium and causing monthly endometrial shedding, progesterone also protects the endometrium.

60
Q

progesterone

A

stimulates 17b hydroxysteroid dehydrogenase and sulfotransferase activities that convert estradiol to estrone sulfate.

61
Q

hypogonadotropic, hypogonadism

A

Hypogonadism is a condition in which the male testes or the female ovaries produce little or no sex hormones. Hypogonadotropic hypogonadism (HH) is a form of hypogonadism that is due to a problem with the pituitary gland or hypothalamus.

62
Q

in cases of prolonged bleeding, any low dose OCs can be used how?

A

bid daily for at least 5-7 days until bleeding slows.

63
Q

if endometrium is denuded, may give

A
  1. 25mg conjugated estrogens or

2. 0 mg micronized estradiol every 4-6hrs x 24 hrx followed by one pill a day for the next 7-10days

64
Q

provera challenge test

A

Progestin challenge, or progesterone withdrawal test is a test used in the field of obstetrics and gynecology in order to evaluate a patient who is experiencing amenorrhea. Due to readily available assays to measure serum estradiol levels, this test is now rarely used.[1] The test is performed by administering progesterone orally in the form of medroxyprogesterone acetate (Provera), or intramuscularly. If the patient has sufficient serum estradiol (greater than 50 pg/mL) then withdrawal bleeding should occur 2-7 days after the progestin is finished, indicating that the patient’s amenorrhea is due to anovulation. However, if no bleeding occurs after progesterone withdrawal, then the patient’s amenorrhea is likely to be due to either a) low serum estradiol, b) hypothalamic-pituitary axis dysfunction, c) a nonreactive endometrium or d) a problem with the uterine outflow tract, such as cervical stenosis or uterine synechiae (Asherman’s syndrome). In order to distinguish between hypoestrogenism or a 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 the amenorrhea is likely due to low estrogen.[2]

65
Q

fertility and gonadal failure

there is no proved method of restoring fertility in POF patients. what labs should draw for POF:

A

ovarian markers such as anti-mullerian hormone (AMH), inhibin B, and antral follciel count may provide more accurate assessment of follicular quantity as compared to FSH alone.

66
Q

for POF, infertility treatments such as gonadotropin stimulation have little if any results

A

true

67
Q

donor oocyte ivf / adoption should be discussed

A

true

68
Q

CHRONIC MENORRHAGIA most common causes

A

anovulation, endometrial distortion (fibroids, polyps, IUDs, tumors), and adenomyosis

69
Q

a __ and __ should be done in everyone who presents with abnormal bleeding why?

A

pregnancy test and pelvic US. most common cause of a sudden change from regular menses is a complication of pregnancy.

70
Q

check CBC to r/o anemia

A

true

71
Q

if __ is confirmed, additional workup includes

A

BMI, FSH, prolactin, TSH, androgens

72
Q

hyperandrogenemia and anovulation should raise suspicion for

A

polycystic ovary syndrome

73
Q

an endometrial biopsy should be performed if

A
  1. a patient is anovulatory and 40 years or older
  2. has had a long duration of exposure to unopposed estrogen regardless of age
  3. is postmenopausal.
74
Q

ANOVULATION results in amenorrhea in 20-30% of the time and ___ in 30% of the time

A

menorrhagia

75
Q

anovulation is abnormal bleeding resulting from prolonged exposure to estrogen - in the absence of progesterone, which leads to an unstable ___.

A

endometrium.

76
Q

most common cause of adult onset anovulation are

A
  1. ovarian dysfunction (50%)
  2. hypothalamic dysfunction 35% - abnormalities in body composition and weight, stress and strenuous exercise.
  3. pituitary disease 15%
77
Q

methods to detect ovulation

A
  1. basal body temperature - prior to ovulation morning bbt 98 a biphasic pattern is almost always associated with ovulation.
  2. Luteal serum progesterone - greater than 3mg/mL always associated with normal seretory endometrium
  3. LH surge - detected by lab values or LH detection kit: ovulation occurs 34-36 hrs after the onset of an LH surge, 10-12 hrs after teh LH peak.
  4. ultrasound changes: follicular growth, rupture and formation of corpus luteum.
78
Q

treatment :

A
  1. oral contraceptives are first line therapy to regulate menses, they are easily tolerated and protect the endometrium.
  2. cyclic progtins are also sufficient to protect the endometrium if OCs are not tolerated or contraception is not desired.
  3. occasionally, bleeding is unresponsive to progesterones / combination oral contraceptives because bleeding may be secondary to a very thin or denuded endometrium rather than a thickened unstable endometrium; in these cases; high dose estrogen therapy can be used in both oral and iV forms: 1.25mg conjugated estrogens or 2.0mg micronized estradiol every 4-6 hrs x 24 hrs followed by one pill a day for the next 7-10days.
  4. Norethindrone IUD (mirena) - significantly decreases menorrhagia.
  5. NSAIDS - decreases prostaglandin synthesis in the endometrium and can reduce blood loss by 20-50%. should be stated on first day of menses and continued for at least 5 days.
  6. antifibrinolytic - more effective than NSaIDS and cyclic progestins in reducing blood flow. only take 1-2 days before menses and for the first 2 days of the menses.
  7. endometrial ablation / destruction of endometrium.
  8. gonadotropin releasing hormone agonists - limit to 6 months to 1 year given risk of irreversible bone loss.