reproductive- related videos (period, hormones) Flashcards

1
Q

functional unit of the ovaries

A

follicles (contain a single oocyte)

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2
Q

describe an ovarian follicle layers

A

oocyte
surrounded by an Antrum (fluid)
inner most layer: granulosa cells
followed by oter most layers: theca cells
NOTE: theca and granulosa synthesize estrogen to drive the growth of the follicle

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3
Q

-pituitary hormones (i.e FSH , LH) level during the 3 phases
-estrogen, progesterone?
sos

A
  • initially low, spike right before ovulatio, fall after
  • estrogen spike right before ovukation, fall after
  • following ovulation (gentle small rise of estrogen and great rise in progesterone level)
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4
Q

mid-cycle surge. explain

when is the oocyte released from a follicle?

A

switch from -ve feedback (rem: high GnRH—> high FSH—> high estradiol —-ve feedback—> decreases FSH/LH) to +ve feedback, where
estradiol triggers increase frequency of GnRH pulses leading to LH SURGE!!
-oocyte released from follicle 36 hrs after LH surge

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5
Q

basis of ovulation testing (when to get pregnant) test. detects what ?

A

urine detection of LH (i.e when its LH surge) thus 36 hrs after an oocyte is released :)

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6
Q

mittelschmerz. when? due to? characteristics? resolution? mimic?

A
  • mid-cycle pain
  • d/t enlargement of follicle or rupture with bleeding :)
  • mild UNILATERAL (on the side where follicle is)
  • resolves in hrs to days
  • mimic APPENDICITIS
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7
Q

when is the corpus luteum formed?

what is it? fxn?

A

-luteal phase
-TEMPORARY endocrine gland formed from the follicle
-produces A LOT of progesterone and some estradiol
by negative feedback this deceases FSH/LH

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8
Q

when does menstruation occur in term of ovulation

A

2 weeks after ovulation

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9
Q

what effect fertilization has on hormonal levels in the ovaries

A

embryo makes hCG

which maintains corpus luteum and progesterone production, thus will maintain suppression of LH/FSH

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10
Q

2 phases of uterine cycle (changes in endometrium)

A
  • proliferative phase: follicular phase of ovary

- secretory phase: luteal phase of ovary

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11
Q

proliferative phases of the uterine cycle

A

endometrial proliferation (stimulated by estrogen)

  • endometrial thickness increases (> x10)
  • growth of glands, stroma, blood vessels
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12
Q

secretory phase of the uterine cycle

A

AFTER OVULATION
progesterone inhibits proliferation
-NUMEROUS SECRETIONS released to PREPARE FOR EMBRYO !
-changges in blood vessels: sososos
** vessels grow and coil
** form SPIRAL ARTERIES about 9th post ovulatory day
(critical for implantation, support of fertilized egg)

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13
Q

physiology of menstruation

A

progesterone levels fall
so vasoconstriction of spiral arteries
leads to APOPTOSIS of endometrial cells !!!!!!!
thus, collapse and desquamation of endometrium

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14
Q

if a women presents with secondary amenorrhea (i.e cessation of normal menses after prior normal periods)
what should we consider? (group of causes)

A

1- PREGNANCY (screen with HCG measurement) most common
2- Hypothalamus, pituitary, other:
—thyroid: BOTH hypo and hyper
—prolactin: prolactinoma (inhibition of GnRH release, thus decreases LH/FSH)
—cortisol: cushing syndrome (high cortisol level)
3- ovary (estrogen/progesterone problems)
4- other
—LOW BODY WEIGHT (functional hypothalamic amenorrhea)
stress plus low caloric intake leads to low GnRH levels thus low LH, FSH
patients RESPOND TO pulsatile GnRH
-can occur in arorexia

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15
Q

what is progestin challenge?
why not used anymore?
how is it done?

A
  • older test for cause of amenorrhea
  • many false +ve
  • administration of progestin (oral/IM) + observe for menstrual bleeding within 7 days
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16
Q

if bleeding occurs after a progestin challenge, indicates what ?
classic cause ?

if no bleeding occurs, indicates what?
common cause ?

A
  • estrogen is present but NO PROGESTERONE
  • classic cause: PCOS (corpus luteum is not forming to make progesterone)

-estrogen not present to proliferate endometrium or anatomic menstrual outflow problem
follow up: estrogen-progestin challenge
common cause: menopause (oestrogen, progesterone, ovulation are absent)

17
Q

girl present with primary amenorrhea

  • normal LH/FSH levels
  • normal estrogen/progesterone levels
A

due to all hormones normal (hypothalamus, pituitary, ovaries must be normal) so:
mullerian dysgenesis (failure of mullerian duct development)
absent upper vagina and/or uterus
(i.e no lining to be shed at puberty)

18
Q

why anoroxic women can get secondary amenorrhea?

tx?

A

—LOW BODY WEIGHT (functional hypothalamic amenorrhea)
stress plus low caloric intake leads to low GnRH levels thus low LH, FSH
-patients RESPOND TO pulsatile GnRH

19
Q

MENOPAUSE IS THE —-

median age?

A

depletion of ovarian follicles !
median age= 51 yrs
women loses estrogen and progesterone coming from the ovaries

20
Q

what is the source of esstrogen after menopause

A

adipose tissue
(aromatase converts androstenedione to estrone)

androstenedione: weak androgen produced by the adrenal gland

21
Q

what is an early finding test in menopause?

A

HIGHH FSH (followed by high LH later on)
due to loss of INHIBIN production from follicles
*inhibin normally suppresses FSH release

22
Q

symptoms of menopause 4

A
all associated with loss of estrogen levels 
1- hot flashes (few mins and passes) 
2- vaginal atrophy (thin, dry, friable) 
3- osteoporosis 
4- CV dxs (risk rises)
23
Q

what tx can be used for menopause symptoms

A

HRT
-(oral or transdermal estradiol)
+progestin (if uterus is intact) to prevent endometrial hyperplasia :)

24
Q

what is the main indication for HRT in menopause?

A

1- relieves HOT FLASHES

and 2- improves bone density

25
Q

risk of HRT 2

A
  • increased risk of stroke, DVT, MI

- increased risk of BREAST cancer

26
Q

how can PCOS cause 2o amenorrhea?

A

genetics + diet/obesity —>increased LH:FSH ratio
so, LH drives production of ANDROSTENEDIONE from theca cells
will be released into serum and some of it will be converted into estrone by adipose tissue.
estrone —> decreases more FSH —> anovulation

27
Q

review PCOS causes and hormones

A

1- genetics + die/obesity lead to:
—-increased LH: FSH ratio
—-hyperinsulinemia
2-high LH drives production of andriostenedione from theca cells
—-normally: andriostenedione should be converted to estradiol (by granulosa cells) but this cant happed d/t low FSH
—-so some of it is converted to testosterone leading to hirsutism/ acne
—-others are converted into estrone (in adipose tissue)
3- estrone further suppress FSH (so there will be anovulation and follicular cysts)
as a result progesterone will be decreased (no normal ovulation)

28
Q

PCOS can lead to diabetes !!!! due to

A

hyperinsulinemia leading to insulin resistance

29
Q

-obese female
-HIRSUTISM (facial hair)
-acne
-amenorrhea
-INFERTILITY
US shows: multiple follicular cysts

A

PCOS

30
Q

how is PCOS diagnosed?

hormone measurements?

A

-clinically
-TOTAL TESTِESTERONE (most reliable indicator)
-LH and FSH normal range
but LH:FSH ratio usually >2:1 !!!!!!!!!!!!!! abnormal (characteristic feature)

31
Q

tx for pcos

A

1- weight loss
2- ORAL CONTRACEPTIVES (suppress LH)
also, estrogen component will increase the SHBG sex hormone binding globulin which will decrease androgens
3- spironolactone blocks androgens
4- metformin/TZDs (improve insulin resistance)
not routinely used !

32
Q

risk of diabetes in PCOS statistics

A

10% by 40 yrs

33
Q

what are acanthosis nigricans?
can they be found in PCOS?
in what diseases are they common?

A

-plaques of darkened skin
-yes, ass with insulin resistance
1- diabetes
2-PCOS
3- gastric cancer

34
Q

PCOS increases the risk of what cancer?why?

A

endometrial cancer (unopposed estrogen) d/t lack of progesterone

35
Q

workup for amenorrhea

sososososo

A
RULE OUT
1- pregnancy 
2- thyroid
3- cushing 
4- prolactin
5- anorexia 
THEN measure FSH: 
low: PCOS (high LH: FSH ratio) 
high: menopause 
normal: mullerian dysgenesis