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Ob-Gyn > The Menstrual Cycle > Flashcards

The Menstrual Cycle Flashcards

1
Q

PMS: h/a, weight gain, bloating, breast tenderness, mood fluctuation, restlessness, irritability, anxiety, depression, fatigue

  • -occur approx 2 wks prior to menstruation
  • -resolve after menstration

1st line tx?

Which OCP is approved for tx?
–combined estrogen + drospirenone

A

PMS Tx: SSRIs

OCP - Yaz
–combined estrogen + drospirenone (a spironolactone with anti-mineralcorticoid and anti-androgenic activity)

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2
Q

s/s menopause to include amenorrhea, hot flashes, mood disturbances, atrophic vaginal mucosa

woman age less than 40

increased FSH/LH, decreased estrogen

often associated with autoimmune disorder

Dx? Tx?

A

Dx: Primary ovarian failure

Tx: IVF

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3
Q

Diagnosis of Menopause

s/s include amenorrhea for 12+ months; hot flashes, mood swings, insomnia, depression, osteoporosis, vaginal atrophy (dyspareunia, dysuria)

What hormonal finding is diagnostic?

What two body systems lose protective benefits from loss of estrogen?

A

Increased FSH
–due to decreased negative feedback from diminished estrogen production

Increased CAD risk
–increased LDL, increased atherogenesis

Increased osteoporosis risk
–increased bone resorption

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4
Q

HRT (E + P combo) can be used to treat menopausal s/s and prevent osteoporosis.
–used short-term with minimal dosage due to cardiovascular risks

Contraindications to HRT

1) re: liver
2) re: cancer
3) re: blood

A

HRT (E + P combo) can be used to treat menopausal s/s and prevent osteoporosis.
–used short-term with minimal dosage due to cardiovascular risks

Contraindications to HRT

1) chronic liver impairment
2) estrogen-dependent neoplasm (breast, ovary, uterus)
3) hx of thromboembolic disease

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5
Q

FSH, LH levels to distinguish…

  1. Menopause
  2. Anovulation due to obesity
  3. Premature ovarian failure
A

Menopause
–increased FSH, LH

Anovulation due to obesity
–normal FSH, LH

Premature ovarian failure
–increased FSH, LH

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6
Q

Menstrual Cycle Physiology

Follicular/Proliferative Phase

  • -FSH stimulates development of ovarian follice
  • -ovarian follicle produces what hormone?
  • -how does this hormone affect uterine lining?

Ovulation
–at midcycle, a spike in what hormone precedes an estrogen surge?

A

Menstrual Cycle Physiology

Follicular/Proliferative Phase (Day 0 to 14)

  • -FSH stimulates development of ovarian follicle
  • -ovarian follicle –> Estrogen
  • -Estrogen –> proliferation of uterine lining

Ovulation

  • -at midcycle, LH spike –> estrogen surge
  • -estrogen surge –> ovulation
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7
Q

Menstrual Cycle Physiology

Luteal/Secretory Phase

  • -remnants of ovarian follicle become the CL
  • -CL secretes what hormone?
  • -how does this hormone affect endometrial lining?
  • -what happens with no fertilization?
A

Menstrual Cycle Physiology

Luteal/Secretory Phase

  • -remnants of ovarian follicle become CL
  • -CL –> progesterone
  • -progesterone –> maintain endometrial lining for implantation
  • -no fertilization –> CL degenerates –> drop in progesterone –> sloughing –> menses
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8
Q

Menstrual Cycle Physiology: Estrogen Production

  1. Theca interna cells of follicle
    - -produce what hormone? in response to stimulation by what hormone?
  2. Theca granulosa cells of follicle
    - -what hormonal conversion occurs? in response to stimulation by what hormone?
A

Menstrual Cycle Physiology: Estrogen Production

  1. Theca interna cells
    - -produce androstenedione in response to LH stimulation
  2. Theca granulosa cells
    - -convert androstenedione to estradiol in response to FSH
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9
Q

Hypothalamic-Pituitary-Ovarian Axis

Estrogen produces negative feedback on what hormone?

Progesterone produces negative feedback on what hormone?

A

Hypothalamic-Pituitary-Ovarian Axis

Estrogen –> neg fdbk on FSH

Progesterone –> neg fdbk on LH

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10
Q

Enzyme responsible for conversion of adrenal androgens to estrogen?

Where is the main site of this conversion during childbearing years?

Where is the main site of this conversion after menopause?

A

Aromatase

  • -converts androgens –> estrogen
  • -present in granulosa cells of ovary

Child-bearing years: ovaries

Post-menopause: adipose tissue
–extra adipose tissue in obese women may mitigate menopausal symptoms

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11
Q

Polycystic Ovarian Disease
–chronic anovulation, oligomenorrhea/amenorrhea, hirsutism, obesity, enlarged polycystic ovaries

Chronic anovulation –> increased E + androgen

Increased androgens

  • -Where are they converted to estrone?
  • -increased ? –> increased free E + androgens

Hyperestrogen state

  • -> increased LH:FSH ratio
  • -> anovulation
  • -the cycle propagates
A

Polycystic Ovarian Disease
–chronic anovulation, oligomenorrhea/amenorrhea, hirsutism, obesity, enlarged polycystic ovaries

Chronic anovulation –> increased E + androgen

Increased androgens

  • -converted to estrone in peripheral adipose tissue
  • -increased SHBG –> increased free E + androgens

Hyperestrogen state

  • -> increased LH:FSH ratio
  • -> anovulation
  • -the cycle propagates

*Hyperthecosis - severe form of PCOS

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12
Q

PCOD: Tx

Tx for fertility?

Tx to prevent endometrial hyperplasia secondary to hyper-estrogen state?

A

PCOD: Tx

Fertility Tx
–clomiphene (ovulation induction)

Prevent endometrial hyperplasia
–progestins, Depo-Provera

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13
Q

Dx:

1) 46, XX; adrenal insufficiency, salt-wasting at birth; females have ambiguous genitalia and normal internal genitalia; normal estrogen levels
2) XX females with ambiguous external genitalia; normal internal genitalia; high testosterone and androstenedione; low or absent estrogen; high FSH and LH; delayed menarche or primary amenorrhea, delayed puberty, osteoporosis

A

1) Congenital adrenal hyperplasia
- -21 alpha hydroxylase deficiency
- -decreased Cortisol –> hypotension, adrenal insufficiency
- -decreased Aldosterone –> salt wasting, hyperkalemia
- -compensatory increased ACTH –> increased 17-OH-P –> increased androgens
- -females have ambiguous genitalia; normal internal genitalia
- -normal estrogen levels

2) Aromatase Deficiency
- -XX female; ambiguous external genitalia; normal internal genitalia
- -primary amennorhea or delayed menarche; delayed puberty, osteoporosis
- -high T/androstenedione; high FSH, LH; low or absent E

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14
Q

Dx:

  1. multiple cystic bone lesions; cafe au lait spots; gonadotropin-independent precocious puberty
  2. congenital absence of GnRH; low or absent FSH/LH; primary amenorrhea; no breasts; uterus present; anosmia
A
  1. McCune-Albright Syndrome
    - -multiple cystic bone lesions
    - -cafe au lait spots
    - -gonadotropin-independent precocious puberty
  2. Kallman Syndrome
    - -primary amenorrhea
    - -no GnRH, low or absent FSH/LH
    - -anosmia
    - -no breasts
    - -uterus present
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15
Q

Secondary Amenorrhea DDx

  1. four initial lab tests? and their associated dx?
  2. two anatomical causes?
A

Secondary Amenorrhea

  1. b-hCG, TSH, prolactin, FSH
    * b-HCG –> pregnancy
    * high TSH –> hypothyroidism
    * high prolactin –> hyperprolactinemia
    * high FSH –> premature ovarian failure
    * low FSH –> hypogonadotropic hypogonadism
  2. Anatomical causes
    - -Asherman syndrome
    - -cervical stenosis
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16
Q

Progesterone Challenge Test
–to asses adequacy of endogenous estrogen production and outflow tract

Positive withdrawal bleed indicates anovulation due to endocrine disorder

Negative withdrawal bleed f/u with E+P admin:

  1. absence of withdrawal bleed following E+P admin
  2. positive withdrawal bleed following E+P admin
    * What do these results indicate with regards to etiology of amenorrhea?
A

Progesterone Challenge Test

Positive withdrawal bleed indicates anovulation due to endocrine disorder.

Negative withdrawal bleed f/u:

  1. outflow tract disorder (cervical stenosis, Asherman syndrome)
    - -absence of withdrawal bleed following E+P admin
  2. inadequate estrogen
    - -positive withdrawal bleed following E+P admin
17
Q

PCOS Pathophysiology

  1. increased GnRH pulsatile activity
  2. Which pituitary hormone is preferentially made?
  3. increased androgen production by theca lutein cells –> hirsutism, acne
  4. low FSH levels –> granulosa cells secrete less estradiol, lack of follicle maturation –> oligomenorrhea, anovulation
  5. What happens to androgens in the periphery?
  6. Levels of SHBG?
A

PCOS Pathophysiology

  1. increased GnRH pulses
  2. increased LH (LH/FSH > 2)
  3. increased androgen production by theca lutein cells –> hirsutism, acne
  4. low FSH –> granulosa cells secrete less estradiol, lack of follicle maturation –> oligomenorrhea, anovulation
  5. peripheral androgens converted to estradiol by aromatase
  6. decreased SHBG + increased peripheral estradiol –> unopposed estrogen exposure to endometrium –> increased risk of endometrial cancer
18
Q

Dysmennorhea DDx

  1. crampy lower abdominal and pack pain during menses; absence of dyspareunia and GI symptoms; normal PEx
  2. pain peaks right before menses; dyspareunia; infertility; uterosacral nodularity and tenderness
  3. heavy menses with clots; constipation; urinary frequency; pelvic pain/heaviness; enlarged uterus
  4. pelvic pain; menorrhagia; bulky, tender and globular uterus
  5. dull, ill-defined pelvic ache that worsens with standing; dyspareunia
A

Dysmennorhea DDx

  1. Primary dysmenorrhea
  2. Endometriosis
  3. Fibroids
  4. Adenomyosis
  5. Pelvic congestion syndrome
19
Q

What is the “female athlete triad?”

A

Female Athlete Triad

  • -amenorrhea
  • -disordered eating (inadequate caloric intake)
  • -osteoporosis
  • seen in severe stress, exercise, anorexia
  • low GnRH, low FSH, low E
  • increased cardiovascular and bone morbidity
20
Q

Dx?

Female teenager; acne, hirsutism, irregular menses; markedly elevated 17-OH-P. No virilization.

A

21-hydroxylase deficiency (partial)

Ob-Gyn (11 decks)

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