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PHS 933 > Block 2 Lecture 3 -- Endometriosis and Amenorrhea > Flashcards

Block 2 Lecture 3 -- Endometriosis and Amenorrhea Flashcards

1
Q

What are the theories for causation of endometriosis?

A

1) retrograde menstrual flow
2) vascular/lymphatic spread
3) immunologic disorder

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2
Q

Where are usual locations of lesions from endometriosis?

A

usually restricted to pelvic cavity

    • ovaries
    • fallopian tubes
    • intestines
    • bladder/uterus
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3
Q

Why do some endometriosis patients experience pain with intercourse and/or bowel movements?

A

adhesions form between organs and restrict movement of organs

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4
Q

How is endometriosis classified? What does the classification mean?

A

Stage I - IV

    • relates to severity
    • does not relate to pain, infertility, or prognosis
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5
Q

What is the primary choice for restoring fertility in endometriosis?

A

laparoscopic surgical treatment

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6
Q

What is the only solution to ondometriosis?

A

ovarectomy +/- hysterectomy

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7
Q

What are the GnRH agonists?

A

Leuprolide IM
Goserelin SQ
Nafarelin IN

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8
Q

What is the MoA of danazol?

A

weakly androgenic steroid that suppresses FSH/LH release; slightly immunosuppressive

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9
Q

What proportion of reproductive women are affected by endometriosis?

A

6-10%

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10
Q

What are the symptoms of endometriosis?

A

1) chronic acyclic or cyclic pelvic pain
+/- dyspareunia
+/- dysmenorrhea

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11
Q

What are the considerations of laparoscopic surgical treatment for endometriosis?

A

best results for tx, but:

– 20% recurrence after 2 years, increasing after that

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12
Q

What are the therapeutic classes indicated for endometriosis treatment?

A

1) NSAIDs or CHC
2) progestins
3) GnRH agonists
4) Danazol

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13
Q

What are the therapeutic classes indicated for PMS treatment?

A

1) antidepressants (SSRIs, TCAs, venlafaxine)
2) GnRH agonists or oral/depot contraceptives
3) diuretics

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14
Q

What is the definition of amenorrhea?

A

absence of menses

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15
Q

Define primary amenorrhea:

A

no previous menses

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16
Q

Define secondary amenorrhea:

A

no menses for 6 months

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17
Q

What is the most common cause of amenorrhea

A

unrecognized pregnancy

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18
Q

Which form of amenorrhea (primary/secondary) is more common – give percentage.

A

secondary = 4% of women

– also more common if

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19
Q

What are the 3 general categories of amenorrhea?

A

1) HT/pituitary suppression
2) anovulatory amenorrhea (PCOS, ovarian tumors, CAH)
3) POI

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20
Q

What are causes of hyperprolactinemia?

A

1) OCs
2) antipsychotics (DAr blockers = haldol, risperidone, chlorpromazine)
3) antidepressants (TCAs, SSRIs)
4) opiates, H2RAs

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21
Q

What is defined as hyperprolactinemia?

A

PRL = 100+ ng/mL

– indicates prolactinoma

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22
Q

Describe feedback loop of PRL release.

A

– HT makes DA

1) PRL from pituitary
2) PRL stimulates DA release from HT
3) DA inhibits PRL (pituitary) and GnRH (HT)

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23
Q

How is menorrhagia defined?

A

excessive bleeding

    • 80+ mL
    • or 7+ days
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24
Q

What are the characteristics of PCOS?

A

1) menstrual abnormalities
2) infertility
3) hyperandrogenism
4) obesity, esp. abdominal
5) symptoms of t2dm
6) acanthosis nigricans
7) U/S shows polycystic ovaries

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25
Q

What is acanthosis nigricans?

A

dark skin at neck, groin, and axillae

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26
Q

What are menstrual symptoms of PCOS?

A

1) amenorrhea
2) menorrhagia
3) acyclic anovulatory bleeding

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27
Q

Why does anovulatory bleeding occur in PCOS?

A

CL does not form = no progesterone = unopposed estradiol

– endometrial hypertropy leads to necrosis and irregular bleeding

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28
Q

What are risk factors for PCOS?

A

1) f/h (25-50% prevalence)

2) central obesity

29
Q

What is the cause of PCOS?

A

genetic, but underlying defect unknown

30
Q

Describe hormonal abnormalities in PCOS.

A

1) LH greater than FSH
2) flat-line LH, slight fluctuation in FSH
3) E 2x greater than P
4) decreased SHBG = elevated FREE T

31
Q

Describe role of adipose in PCOS.

A

converts androgen into estrone

32
Q

What is the function of leutinizing hormone?

A

1) stimulate androstenedione production in ovaries

2) surge converts follicle into corpus luteum

33
Q

What are estrone’s effects on the pituitary?

A

increased LH release

34
Q

What are the goals of therapy in PCOS?

A

1) reduce ovarian androgen secretion, restore hormonal cycle

2) reduce insulin resistance

35
Q

PCOS increases risk for these diseases.

A

1) T2DM/metabolic syndrome
2) dyslipidemia
3) CV disease

36
Q

What are treatment classes for PCOS?

A

1) COCs (progestin only may be appropriate)
2) Metformin/TZDs
3) glucocorticoids or spironolactone/flutamide for anti-androgenic activity
4) clomiphene or metformin for infertility

37
Q

What are the FDA-approved PCOS treatments?

A

1) COCs

2) metformin

38
Q

How is POI defined?

A

in women less than 40 yo…

    • sex steroid deficiency
    • amenorrhea
    • infertility
39
Q

POI increases your risk for what other diseases?

A

osteoporosis, CVD

40
Q

When is the usual onset of POI?

A

after establishment of menses

    • after d/c COCs
    • post-partum
41
Q

How is POI diagnosed?

A

1) 4+ months of amenorrhea

2) FSH = 40+ IU/L

42
Q

What are symptoms of POI?

A
    • 50%: oligomenorrhea or anovulatory bleeding
    • vasomotor sxs
    • mood changes
43
Q

What are causes of POI?

A

autoimmune diseases, genetic defects

    • Turner Syndrome
    • Fragile X
44
Q

What percentage of POI patients get pregnant?

A

5-10%

45
Q

What are causes of HT/pituitary suppression?

A

1) pituitary disease/tumor
2) idiopathic
3) anorexia
4) low-body fat (exercise, weight loss)
5) obesity
6) hyper/hypothyroid
7) hyper-PRL

46
Q

What are causes of anovulatory amenorrhea?

A

PCOS
ovarian tumor
CAH (excessive androgen)

47
Q

What are causes of POI?

A

1) genetic
2) autoimmune
3) idiopathic

48
Q

What are the hormone changes present in POI?

A

low E, high FSH

49
Q

What are ADRs of danazol?

A

androgenic:
- - weight gain
- - acne
- - vasomotor sxs
- - hirsutism
- - more LDL

50
Q

What are C/I’s of danazol?

A

hyperlipidemia, liver disease

TERATOGEN

51
Q

What are ADRs of GnRH analogs?

A
    • 5% bone loss over 6 months (reversible)
    • vasomotor sxs
    • insomnia
    • vaginal dryness
52
Q

What are special counseling points of GnRH agonists?

A

1) supplement with Ca (500-1000 mg/day) + exercise

2) add-back E/P/BP therapy can limit ADRs

53
Q

What is the MoA of GnRH agonists in endometriosis

A

inhibit FSH/LH to establish anovulatory state

54
Q

What is the MoA of progestins in endometriosis?

A

establish anovulatory state with amenorrhea

55
Q

What is the MoA of CHCs in endometriosis?

A

cyclic: hypoestrogenic
continuous: anovulatory; suppress menstruation; prolonged infertility

56
Q

What is the black-box warning on progestins?

A

2-year limit (BMD)

57
Q

How is hypothalamic amenorrhea treated?

A

estrogens +/- progestins

– OCs, CEE, E patch

58
Q

How is hyper-PRL amenorrhea treated?

A

cabergoline 2 x/week

59
Q

Why are spironolactone/flutamide used in PCOS?

A

used with COCs

    • neither FDA approved
    • used to antagonize androgen receptor
60
Q

Why are glucocorticoids used in PCOS?

A

low-dose qhs suppresses adrenal androgens

    • does not restore fertility
    • not FDA approved
61
Q

What are the progesterone-only options in PCOS?

A

1) oral medroxyprogesterone (po x 12-14 days)
- - no contraception
- - not FDA approved
2) levonorgestrel IUD
- - contraception

62
Q

When are progestins contraindicated in PCOS?

A

breast/cervical/uterine/vaginal cancer
thrombembolic disease
stroke

63
Q

When might progesterone-only tx be advantageous in PCOS?

A

if menorrhagic

– amenorrhea likely in 6 months

64
Q

What progestin is preferred in PCOS?

A

desogestrel (least androgenic)

65
Q

Why are COCs used in PCOS?

A

1) restore hormonal cycle
2) increase SHBG to decrease free T
3) reduce ovarian hormone production

66
Q

What is clomiphene’s moa?

A

estrogen receptor antagonist to increase FSH and LH to stimulate ovulation
– acts on HT to increase GnRH pulses

67
Q

How is clomiphene dosed?

A

50 mg/day x 5 days beginning on days 3-5

    • after MPA to induce withdrawal bleed
    • up to 250 mg/day
68
Q

How is POI treated?

A
    • low-dose E increasing to 1.25 mg/day CEE
    • progestin for 12-14 days
    • +/- T for BMD/libido
69
Q

Why is low-dose E used in POI?

A

to re-establish baseline ovarian function

– does not prevent ovulation: you already have elevated FSH/LH

PHS 933 (14 decks)

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