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Menstrual Cycle Flashcards

1
Q

What is the Age range of the Menstrual Cycle?

A

Begins around age 12 and ends around age 50

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2
Q

How many days can a Cycle be? what is the Avg?

A

21-40 days, AVG = 28

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3
Q

Which phase is most likely to vary?

A

Follicular Phase

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4
Q

What is the Follicular phase?

A

single Primary follicle matures, Follicle also ruptures to release oocyte at ovulation.

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5
Q

What is the Luteal Phase?

A

Remaining follicle becomes Corpus Luteum, Uterine endometrium breaks down –> menstruation.

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6
Q

Which two gonadotropins regulate the menstrual cycle?

A

FSH and LH.

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7
Q

What is the make up of FSH and LH and where are they secreted from?

A

Glycoprotein hormones both have a common alpha unit with a unique beta unit. They are secreted by the anterior pituitary.

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8
Q

Which has a longer half life FSH or LH?

A

FSH (3-4hrs) (LH = 20min)

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9
Q

What does FSH do?

A

Stimulates granulosa cells
Facilitates estrogen production
stimulates spermatogenesis

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10
Q

How does FSH facilitate estrogen production?

A

It upregulates aromatase (CYP19)

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11
Q

What does LH do?

A

Stimulates ovulation.
“LH surge” right before oocyte release.
Testosterone production

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12
Q

Where are the places LH acts to stimulate Testosterone production?

A

Follicle thecal cells.

Leydig cells in Testes.

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13
Q

What hormone controls the release of FSH and LH? Where is it also released from?

A

Gonadotropin-releasing Hormone.

Hypothalamus

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14
Q

What are two things the maturing follicle secretes?

A

Estradiol and Inhibin.

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15
Q

What is the most potent of the natural estrogens?

A

Estradiol.

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16
Q

What kind of hormone is Inhibin?

A

Peptide dimer hormone.

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17
Q

What is the result of increased Estradiol and Inhibin? what is the mechanism to obtain the result?

A

Decreased FSH levels.
Estradiol Suppresses GnRH release.
Inhibin Suppresses FSH release.

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18
Q

What are other actions of Estradiol?

A

Stimulate endometrial regeneration.

Promotes cervical mucus good for sperm.

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19
Q

What causes LH surge and how?

A

Estradiol levels >200 pg/ml for >48hr.
High estradiol levels reverse suppression LH release.
Estradiol can act DIRECTLY on pituitary gland.

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20
Q

What produces Progesterone?

A

Corpus Luteum

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21
Q

What are the main functions of Progesterone?

A

Prepeare endometrium for implantation of embryo.

Suppresses GnRH release.

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22
Q

What happens when LH Levels drop?

A

Corpus Luteum degenerates.

Progesterone released from CL –> Menstruation

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23
Q

When are Progesterone levels generally the highest?

A

During Pregnancy (100-200 ng/ml)

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24
Q

Where is the embryo implanted post fertilization?

A

Endometrium.

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25
Q

What happens immediately after fertilazation.

A

The blastocyst (embryo) secretes human chorionic gonadotropin (hCG)

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26
Q

How soon can hCG be detected?

A

6-8 days post fertilization.

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27
Q

What similarities do hCG and LH have?

A

They both maintain the corpus luteum.

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28
Q

When does the placenta begin producing progesterone and Estriol (E3)? What is this process refereed to as?

A

Around 12 weeks after fertilization.

“Luteal-Placental Shift”

29
Q

Why do progesterone levels continue to rise?

A

So the fetus can use it to synthesize glucocorticoids and sex steroids.

30
Q

What is Estriol produced from and when is it most prominent?

A

Produced from estradiol or estrone and ONLY during pregnancy.

31
Q

What happens to levels of progesterone just before birth? What are theories of why?

A

The levels fall dramatically.

Could be signal to induce labor.
Progesterone suppresses contractility.
Progesterone suppresses maternal immune response to fetus.
Inhibits lactation.

32
Q

How many natural estrogens are there?

A

3 types (Estrone, Estradiol, Estriol)

33
Q

What are the characteristics of Estrone?

A

(E1) It is the most abundence post-menopause. Main sources is FAT.

34
Q

What are the characteristics of Estradiol?

A

(E2, 17beta-estradiol)
Most abundant in reproductive women.
Most POTENT
Main source is Ovaries.

35
Q

What are the characteristics of Estriol?

A

(E3)
Most abundant estrogen in pregnancy.
Generated from DHEA (most abundant steroid)
Main source is Placenta.

36
Q

What is common in the synthesis of the estrogens?

A

They all are derived from other steroids and use CYP19 Aromatase.

37
Q

If Estriol is produced from either Estrone or Estradiol, where is it produced?

A

In the liver.

38
Q

If Estriol is produced directly from 16alpha-OHDHEA where is it produced?

A

In the Placenta.

39
Q

What is the mechanism of action for all the Estrogens?

A

Estrogens bind to the Intracellular Estrogen Receptor (ERalpha) which alters gene transcription.

40
Q

What tissues do Estrogens primarily target?

A

Ovaries, Uterus, Breast.

41
Q

What are the Non-Menstrual effects of estrogen?

A

Promote development of secondary sex charc.
Decreases bone resorption/increases formation
Lower LDL, Increase HDL, opposes aldosterone
Positive mood, neuroprotection, softer skin, increased liver proteins and coagulation factors.

42
Q

How many natural Progestogens are there?

A

Progesterone and 17alpha-hydroxyprogesterone.

43
Q

Which progestogen is the main one?

A

Progesterone is the principle circulating one.

44
Q

Where is progesterone formed?

A

Corpus luteum and adrenals.

45
Q

What is the level of progesterone in the luteal phase?

A

10-15 ng/ml

46
Q

Where is 17alpha-hydroxyprogesterone formed?

A

Primarily in the Adrenals.

47
Q

When are there elevated levels of 17alpha-hydroxyprogesterone.

A 
During pregnancy.
In CAH (diagnostic for defective CYP21).
48
Q

What is the level of 17alpha-hydroxyprogesterone in the luteal phase and the 3rd trimester?

A

1-5 ng/ml in Luteal

up to 30 ng/ml in 3rd trimester.

49
Q

What are the two progestogens intermediates for?

A

Glucocorticoids and mineralcorticoids.

50
Q

What is the mechanism of action for progestogens?

A

Progestogens bind to intracellular progesterone receptors (PR) which alters gene transcription.

51
Q

Does progesterone always bind to a PR?

A

No, Progesterone can bind to other sites and cause non-transcriptional effects.

52
Q

What are the primary targets for Progestogens?

A

Uterus, Breasts.

53
Q

What are the Non-Menstrual effects of Progestogens?

A

Progesterone alters sperm motility and may serve as an “attractant” .
Progesterone is likely a “neurosteroid”

54
Q

What is Dysmenorrhea?

A

The “crampy” pelvic pain associated with menstruation.

55
Q

What is the onset of Dysmenorrhea?

A

Typically 1-3 days before menses. Interferes with normal daily activity. (not just menstrual pain)

56
Q

What are possible accompanying symptoms of Dysmenorrhea?

A

Heavy blood loss, nausea, vomiting, headache.

57
Q

What is Primary Dysmenorrhea?

A

Thought to be because release of prostaglandins and leukotrienes.

Cause contraction of uterus, tissue hypoxia, pain.

stronger more frequent contractions.

58
Q

What is Secondary Dysmenorrhea?

A

Most common cause is endometriosis.

Also uterine polyps, pelvic infections, cervical stenosis.

59
Q

What is endometriosis?

A

When growth of endometrial cells outside the uterus.

60
Q

What is the prevalence of Dysmenorrhea?

A

Approx. 25% of women, most common in teens and 20’s. In adolescents est. 70-90%.

Childbearing may reduce incidence.

61
Q

What is the nonpharmacologic treatment of Dysmenorrhea?

A

Topical heat
Exercise
low-fat/vegetarian diet.

62
Q

What is the Pharmacologic treatment of Dysmenorrhea?

A

1) NSAIDS first line.
Begin 1 day prior to onset of menses.

2) Oral contraceptives
decrease endometrial proliferation

3) Depot medroxyprogesterone (MPA)
Causes amenorrhea (loss of cycle)

4) Levonorgestrel IUD
Reduces incidence by 50%
Suppresses endometrial proliferation
Amenorrhea in as many of 60%

63
Q

What is Premenstrual Syndrome (PMS) characterized by?

A 
Mood swings, depression, anxiety, insomnia.
appetite changes
join/muscle pain
headache
weight gain/fluid retention
breast tenderness, acne
64
Q

What is the incidence of PMS?

A

75%
Most common in women age 25-35
Onset 1-2 weeks prior to menses.

65
Q

What is Premenstrual Dysphoric Disorder (PMDD)?

A

Severe PMS
Severe depression, hopelessness, irritability.
may be associated w/ psychiatric disorders
3-8% patients w/ PMS

66
Q

What are 3 categories of treatments for PMS/PMDD?

A
  1. Lifestyle changes
  2. Antidepressants
  3. Hormonal Treatments.
67
Q

What lifestyle changes may help PMS/PMDD?

A
  1. Decreased caffeine, alcohol, sugar, salt
  2. Increased exercise.
  3. Vit. B6 (50-100mg/d), Ca
68
Q

How can antidepressants help treat PMS/PMDD?

A
  1. SSRIs are very effective (1st choice)
    given continuously, only during luteal phase, or w/ onset of symptoms.
  2. Tricyclic antidepressants (clomipramine)
  3. Venlafaxine
69
Q

What Hormonal treatments can be used for PMS/PMDD?

A
  1. GnRH agonists/antagonists.
    - Suppress release of FSH/LH, decrease symptoms
    - Antiestrogenic effects limit use
  2. Oral/Depot Contraceptives
    - Effective by stabilizing hormonal swings
    - can cause same effects as luteal phase.

Endocrine (9 decks)

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