Female menstrual cycle Flashcards

Dr. Pond

1
Q

Where does the development of female gametes occur?

A

Follicles
(starting during the prenatal development of the female)

millions of primordial follicles are formed
only 400-500 are released during reproductive years

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2
Q

Types of Follicles

Follicle development

A

-Primordial follicle
-Primary follicle
-Graafian follicle (mature follicle)
-Corpus luteum

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3
Q

What is the difference between the Primordial and Primary follicle?

A

Primordial follicle: one layer of squamous-like follicle cells surrounding the oocyte

Primary follicle: one or more layer of cuboidal cells surround the oocyte

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4
Q

After 1 week of maturation, which hormone is secreted by the dominant follicle

A

Estrogen

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5
Q

Which hormone drives the development of the follicles?

A

GnRH -> FSH (follicle-stimulating hormone)

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6
Q

Function of estrogen at day 7

A

Negative feedback

inhibition of GnRH release -> low FSH
-so other the follicles lose hormonal support and degenrate (atresia)

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7
Q

Function of estrogen at day 14

A

Positive feedback

stimulates GnRH release -> causing a surge in FSH/LH release

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8
Q

What is the function of LH at day 14

A

after the surge of FSH/LH

LH causes the follicle to rupture -> OVULATION
the ruptured follicle becomes the Corpus luteum

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9
Q

What is the function of the Corpus luteum?

A

It secretes estrogen, progesterone, and inhibin

-> inhibits GnRH and FSH/LH release -> thereby preventing the maturation of new follicles since FSH is needed for maturation

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10
Q

What triggers the restart of the menstrual cycle?

A

The corpus luteum degenerates if fertilization doesn’t occurs -> levels of estrogen, progesterone and inhibin decrease
-> No negative feedback on GnRH

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11
Q

What is the effect of estrogen on the endometrium?

A

it causes the endometrium to become proliferative (the cells divide, it becomes thick)

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12
Q

What is the effect of progesterone on the endometrium?

A

-opposes the proliferative effect of estrogen, so the endometrium doesn’t grow too much

-causes the endometrium to become secretory (providing nutrition)

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13
Q

What happens if a signal for pregnancy is received?

A

release of hCG (until the 1st trimester)
-> prevents degradation of the corpus luteum
-> continued release of

estrogen (endometrium stays proliferative, negative feedback on GnRH)

progesterone: opposes estrogen and keeps the endometrium secretory

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14
Q

Which form of estrogen is mainly produced by the ovary?

A

Estradiol (E2)

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15
Q

What are the hepatic effects of estrogen in the liver?

A

-increased synthesis of clotting factor

-increased synthesis of angiotensin I -> increase in blood pressure

caused by the reabsorption of conjugated metabolites of estradiol (enterohepatic circulation), especially when estrogens are taken orally

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16
Q

Estrogen effects in puberty

A

-Development of vagina, uterus, uterine tubes

-Secondary sex characteristics:
growth of breasts, closing of the epiphysis of long bones, axillary and pubic hair, distribution of body fat, hyperpigmentation of skin (areolae, genitals)

17
Q

Other Estrogen effects in puberty

A

-Uterine: hyperplasia of endometrium, watery cervical mucus
-Skeleton: normal skeletal development, antiresorptive (opposes bone breakdown)

-Cardiovascular system: function of blood vessels
-triglycerides and lipoproteins: elevate HDL, decrease LDL and cholesterol
-Liver: increase CBG,
TBG, SHBG, increase clotting factors,
angiotensinogen

-Blood coagulation
-CNS: cognition and memory, mood
- colon, urogenital tract, eyes

18
Q

Which subtype of estrogen is Estrogen-receptor selective?

A

Estetrol

Nuclear ER-alpha - agonist
Membrane ER-alpha antagonist

19
Q

What are SERMs?

A

-Selective estrogen receptor modulators (bind to estrogen receptors)

-Inhibit ER activity in some tissues/ increase it in others

20
Q

Tamoxifen and cancer

A

when Tamoxifen binds to the receptor it does not cause a change in the shape of the receptor -> the receptor is not able to bind to coactivators

21
Q

Effects and use of Tamoxifen

A

-Antagonist in the breast (used in breast cancer)
-Agonist in uterus and bone

-Reduced risk of atherosclerosis
-black box warning: uterine malignancies and clot risk

22
Q

Effects and use of Raloxifen

A

-Antagonist in breast
-Similar to tamoxifen, but no detectable agonist activity in uterus

-Similar effects as estradiol on lipids and bone
-Used for postmenopausal osteoporosis
-Breast cancer prophylaxis

-ADE: clot risk

23
Q

Effects and use of Clomiphene

A

-Partial agonist in hypothalamus/pituitary

-Long-term binding of ER (weeks) results in
downregulation in ERs -> no negative feedback -> GnRH release -> FSH/LH release

24
Q

How do Progesterone antagonists work?

A

-Progesterone is needed for pregnancy (keeps endometrium secretory)

-Progesterone antagonists block progesterone receptors

-can terminate pregnancies in the first 7 weeks (95% of women)

-used with prostaglandins (stimulates contractions which helps with the shedding)

-ADE: delayed ovulation in the following cycle, prolonged bleeding

25
Q

MOA of combination pills

A

-negative feedback to pituitary -> low level of FSH/LH -> inhibit OVULATION

-change in cervical mucus (progesterone makes it more sticky and harder to penetrate)

-uterine endometrium (it doesn’t become thick and secretory, bc levels of estrogen and progesterone are kept low due to negative feedback)
-> can be helpful for women having heavy bleeding due to too much estrogen -> too thick endometrium -> heavy bleeding

motility and secretion in uterine tubes (due to low levels of progesterone)

26
Q

How does Progestin alone work?

A

prevention of pregnancy

-inhibit ovulation (only 85%) during follicular phase

-increase viscosity in cervical mucus
-atrophic (decrease) uterine endometrium
-decrease motility and secretion in uterine tubes

27
Q

Which contraceptive might be appropriate for breastfeeding patients?

A

Only progesterone

because estrogen may suppress lactation

28
Q

Which contraceptive might be appropriate for patients who struggle with acne?

A

-progesterone without androgenic effect

-progesterone with estrogen (estrogen opposes the androgenic effects of progesterone)

29
Q

What are the severe ADE of contraceptives?

A

-Thromboembolism: 3x risk (estrogen)
-MI
-stroke (estrogen)

-cholestatic jaundice (progestin)
-depression
-cancer

30
Q

How does the drug Phexxi work?

A

-contraceptive vaginal gel (lactic acid, citric acid, potassium bitartrate)
-makes the pH in the vagina acidic so that sperm won’t survive

-ADE: burning sensation, UTI, dysuria, vaginal pain