midterm #2

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if antibodies were directed against TSH receptor, what 2 outcomes could it have on receptor activation? what do these outcomes depend on?

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reproduction: two cell theory, menstrual cycle & metabolism, pregnancy & parturition, lactation

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if antibodies were directed against TSH receptor, what 2 outcomes could it have on receptor activation? what do these outcomes depend on?

  • depending on where antibodies bind on TSH receptor, can either:

    • stimulate, so receptor consistently activated → G protein signal

    • block, so receptor inactivated and cannot be activated → G protein blockade

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if someone’s bodies starts making antibodies directed against the TSH receptor, to the point of blockage, what would happen to:

  1. follicular cells of thyroid?

  2. T₃/T₄ production?

  3. TSH levels?

  4. symptoms?


  1. ↓ b/c blocked receptors → no TSHR activation → ↓ follicular cell size

  2. ↓ b/c TSHR on anterior pituitary cells blocked

  3. ↑ b/c ↓ T₃/T₄ causes negative feedback

  4. ↓ lipolysis (obesity), indigestion, feeling cold

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what are the 2 main types of hypothyroidism pathologies?

  • primary, secondary, tertiary, or peripheral hypothyroidism

  • impact (cretinism), myxedema

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what are the 3 main types of hyperthyroidism pathologies?

  • Graves disease

  • thyroid adenoma

  • exogenous T₃/T₄

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how does the outcome of hypothyroidism differ between neonatal vs. later in life?

fatal vs. ok

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what are some symptoms of hypothyroidism, especially as its indicative of slowed metabolism? what age group are these symptoms most common in?

fatigue, cold, ↓ HR, muscle weakness, dry skin/hair, anemia, constipated; very common with elderly

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describe primary hypothyroidism. what are the 3 possible causes for it?

  • primary = issue with thyroid gland itself

    • Hashimoto’s thyroiditis

    • thyroid ablation (removal)

    • low levels of iodine intake

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describe Hashimoto’s thyroiditis. what 3 factors are inhibited in thyroid mechanisms?

autoimmune antibodies that go against: Tg, TPO, or TSH receptors

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in Hashimoto’s thyroiditis, if Tg or TPO weren’t made, what would happen to levels of TSH and why? would goiter be present?

no Tg/TPO → ↓ T₃/T₄ produced → ↑ TSH via negative feedback; → TSH receptor activation → ↑ follicular cell size → goiter

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when does goiter happen in Hashimoto’s thyroiditis? why? what happens to thyroid eventually, along with T₃/T₄ production?

early stages as TSH tries to rescue prod. of T₃/T₄; eventually, thyroid destroyed → no T₃/T₄ prod.

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in secondary hypothyroidism, where is the issue? what is the effect on T₃/T₄ production?

issue with anterior pituitary (adenoma or damage); less TSH prod. → ↓ T₃/T₄ production

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in tertiary hypothyroidism, where is the issue? what is the effect on T₃/T₄ production?

problem in hypothalamus; ↓ TRH → ↓ TSH → ↓ T₃/T₄ prod.

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describe myxedema. is this associated with short or long-term hypothyroidism? what is accumulated because of what low activity? what are its symptoms?

  • accumulation of mucopolysaccharides subcutaneously b/c low degradation enzyme activity; associated with long-term hypothyroidism

    • symptoms: thick and doughy skin, puffy face around eyes, hoarse voice

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if hypothyroidism occurs in utero/infancy, what can the baby develop? what are its symptoms? what treatment can be done, and can the baby be saved with what conditions?

  • cretinism; short stature with underdeveloped bones, cognitive impairment with lack of T₃/T₄ for CNS development

    • early treatment with synthetic T₄ can return development to normal; if not treated early, then die

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what is a general treatment for hypothyroidism? what does this mean for prognosis?

synthetic T₄ (levothyroxine); thus, treatment is accessible and can recover development if treated early

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describe subclinical hypothyroidism. what are the conditions for T₃/T₄ vs. TSH levels? why should this be treated?

  • when T₃/T₄ = normal, but TSH = elevated; so, T₃/T₄ is less than usual in situation

    • should be treated b/c elevated TSH levels → ↑ cardiovascular disease (mortality)

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how is subclinical hypothyroidism treated? how does this work?

treatment with synthetic T₄ (levothyroxine), which neg. feedback to ↓ TSH while maintain T₃/T₄ levels in normal range → ↓ cardiovascular risks

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if antibodies were generated against TSH receptors such that it activates them, what happens to:

  1. T₃/T₄ levels?

  2. TRH? TSH?

  3. goiter?

  4. symptoms?


  1. ↑ T₃/T₄ b/c TSHR activated

  2. both ↓ b/c neg. feedback from ↑ T₃/T₄

  3. yes b/c TSHR activation ↑ (despite low TSH)

  4. ↑ metabolism, so weight loss, ↑ HR, and hot flashes

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define thyrotoxicosis. what pathology is this usually associated to?

accelerated metabolism in organ systems with hyperthyroidism (↑ circulating thyroid hormones)

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what mostly causes hyperthyroidism?

hyperactive thyroid gland; primary

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describe some symptoms of hyperthyroidism, especially as it related to increased metabolism.

↑ temp., weight loss, diarrhea, sweaty skin, ↑ HR

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describe Grave’s disease and how it causes hyperthyroidism. how does this affect TRH and TSH?

autoimmune antibodies that bind onto TSH receptors → perpetual activation → ↑ T₃/T₄ prod. → ↓ TRH and TSH via neg. feedback

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what type of goiter is presented from Grave’s disease?


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what 3 subpathologies develop from Grave’s disease? briefly describe each.

  • exopthalamus: antibody actions (inflammation) on extra ocular muscles (phenotypically, bulging eyes)

  • dermopathy: thick, discolored skin on shin

  • oncholysis: nail bed lifting

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describe thyroid adenoma and how it causes hyperthyroidism. in a RAIU (radioactive iodine uptake) test, how do thyroid body vs. nodules visually compare?

  • tumor nodule that prod. ↑ T₃/T₄ → low TSH

    • most thyroid = cold, but nodules come out as hot → super active via ↑ I⁻ usage

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how does thyroid adenoma symptoms compare with Grave’s disease? what does this indicate about the former?

no symptoms typical of Grave’s disease; thus, this results from autoimmune condition

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describe nodular goiter. where is swelling localized? what can it be due to?

focal areas of swellings, can be spread across vastly across thyroid; prod. excess T₃/T₄ b/c tumors or regional hyper-responsiveness to TSH

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describe pituitary adenoma. what is its cause? what type of goiter does it produce?

  • ↑ TSH prod. from pituitary → ↑ T₃/T₄

    • also, ↑ TSH → ↑ TSHR activation → diffuse goiter

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describe treatment for Grave’s disease vs. adenoma.

  • Grave’s disease (hyperactive thyroid): treated with PTU (block organification → ↓ T₃/T₄ prod. and release) or radioactive I⁻

  • adenoma: removal of source

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what is an issue associated with ablating the thyroid?

may kill too much of thyroid → hypothyroidism

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why are iodine tablets taken in a nuclear fallout?

supplementary iodine that outcompetes radioactive iodine; shuts down thyroid momentarily and lives off of T₃/T₄ stores instead

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define the abbreviations: GnRH, FSH, LH.

  • GnRH = gonadotropin-release hormone

  • FSH = follicle-stimulating hormone

  • LH = luteinizing hormone

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between LH and FSH, which stimulate gonad endocrine cells, which then results in what production? which stimulate gamete production? what sex exception is featured with the latter?

  • LH → endocrine cells → sex steroid and peptide hormones → gamete prod.

  • FSH → gamete prod. directly

    • however, in female only, both LH and FSH stimulate gamete prod. directly

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what type of feedback by hormones secreted by gonads is featured onto hypothalamus and pituitary?


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where are GnRH neurons located? what system takes GnRH to anterior pituitary?

@ ARC, or arcuate nucleus of hypothalamus; portal system takes GnRH to ant. pit.

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if GnRH-secreting cells don’t have any sex steroid hormone receptors, how do sex steroids feedback signal changes in GnRH levels? what other set of cells are there?

KISS neurons feedback instead

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describe how KISS neurons stimulate GnRH neurons. what is released by them to activate GnRH neurons? where are they located?

KISS neurons (also in ARC) release KISS peptin upon stimulation → activate GnRH neuron to eventually stimulate FSH/LH release

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from the gonads, what negatively feedbacks KISS neurons to decrease release of FSH/LH?


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if testosterone levels were heightened, what would happen to FSH/LH levels? gamete production? explain.

  • ↑ testosterone → ↓ KISS peptin → ↓ GnRH → ↓ FSH/LH

    • gamete prod. needs BOTH androgens AND FSH/LH to produce gametes; thus, ↓ FSH/LH → ↓ gamete prod.

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for testicles, what cells do LH and FSH stimulate respectively?

  • LH → Leydig cells

  • FSH → Sertoli cells

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for ovaries, what cells do LH and FSH stimulate respectively?

  • LH → inner theca cells

  • FSH → Granulosa cells

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what are gonads?

organs that prod. gametes

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describe the direction of sperm growth and development in seminiferous tubules.

start as progenitor cells at basal layer, then move towards lumen as spermatids, then sperm that travel through lumen on tubules

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describe how the 2 cell theory intertwine with each other in spermatogenesis function. where are Leydig vs. Sertoli cells located in a seminiferous tubule? what stimulates each cell to do what?

  1. LH stimulation → Leydig (interstitial; outside of tubule) cells prod. testosterone

  2. FSH and testosterone stimulation → Sertoli (inside of tubule) cells prod. products that aide sperm prod.

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what type of signaling cascade does LH stimulation do to Leydig cells (also, what G protein is involved)? what does this cascade stimulate the expression and activity of?

LH stimulation on Leydig cells → cAMP cascade (Gs protein) → ↑ StAR expression and activity

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what is the immediate function of StAR? what is the final product?

StAR takes cholesterol from outer mitochondrial membrane into inner mitochondrial membrane → eventually prod. testosterone (from mitochondria → smoother ER)

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if a compound blocks adenylate cyclase (AC), what will this do to testosterone production? why?

LH → cAMP cascade (includes AC) → StAR expression → testosterone prod.; no AC → no testosterone

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what 2 things stimulate Sertoli cells?

FSH and testosterone

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what G protein is involved with FSH stimulation? what 3 things is produced from this stimulation?

  • FSH stim. → Gs protein → prod.:

    • inhibin

    • estradiol

    • sperm

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what do inhibin from Sertoli cells do? what and where does it ONLY act on?

neg. feedback on FSH secreting cells of pituitary, only inhibiting FSH (@ anterior pituitary)

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if Sertoli cells released elevated levels of inhibin, what would happen to:

  1. sperm production?

  2. androgen production?

  3. GnRH production?


  1. ↑ inhibin → ↓ FSH → ↓ spermatogenesis @ Sertoli cells

  2. no change b/c androgen prod. is stimulated by LH, and inhibin only inhibits FSH

  3. no change b/c inhibin acts on anterior pituitary (FSH), not hypothalamus

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if Sertoli cells need testosterone for spermatogenesis, what does testosterone do to Sertoli cells? what does it specifically do to assist spermatogenesis? what kinases are involved?

testosterone signaling required for mature sperm release from Sertoli cell membranes; testosterone stimulates androgen receptor → tyrosine kinases cleave tethering proteins → sperm release

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what is the only thing that can negatively feedback onto anterior pituitary and hypothalamus, lowering GnRH, FSH, and LH?


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name some secondary sex effects of testosterone.

  • body/facial hair growth

  • bone growth and epiphyseal closure

  • muscle development

  • acne

  • ↑ libido

  • penile/clit growth

  • ↓ HDL

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what are the gonads for AFAB? what are their gametes called?

ovaries with oocytes

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where are oocytes located within?

follicles in ovaries

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what are the cells that surround the oocyte as a layer? what are the glycoproteins that also surround the oocyte?

granulosa cells, zona pellucida

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what are the 2 recruitment phases of follicle maturation? which is hormone dependent vs. independent?

  1. initial recruitment: hormone-independent

  2. cyclic recruitment: hormone-dependent (FSH)

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in the initial recruitment phase, what is the beginning follicle stage at birth? when do secondary follicles start to develop?

start with primordial follicle, then secondary stage hits when puberty

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how long does it take for a follicle to go from primordial to ovulation post-puberty?

around 1 yr

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how are corpus lutea formed?

after ovulation (release of oocyte), follicle becomes bunds of cells and nutrients without oocyte = corpus lutea

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given a normal vs. no-FSH-receptor follicle, which would have more secondary follicles? corpus lutea? explain.

  • normal: less secondary follicles, presence of corpus lutea

  • no-FSHR": more secondary follicles, absence of corpus lutea

    • this is b/c FSH is needed for secondary follicles to become tertiary; without them, ovulation wouldn’t occur, and corpus lutea would not form

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with this, is FSH required for fertility?

FSH needed for fertility b/c absence prevents ovulation (evidenced by lack of corpus lutea in no FSHR follicles)

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is FSH required for development of follicles?

not necessarily, as no-FSHR follicles were able to develop primary to secondary follicles; but, need FSH for development post-secondary stage (secondary to "“preovulatory”)

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describe development of primary follicle with oocyte size, zona pellucida, and FSH receptor presence.

  • oocyte enlarges with expanding granulosa cell layer

  • zona pellucida appears

  • first see FSHRs

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describe secondary follicle development. what type of cells now start to appear?

granulosa cells continue to divide, and theca cells now present

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in tertiary follicle development, what is now present? what is this full of?

antrum, which is full of hormones

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how many late tertiary/pre-ovulatory cells are made at a time? how big are they?

one per monthly cycle, around 15~25mm

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what hormone activates inner theca cells? through what cascade? what is this similar to?

LH activate inner theca cells via cAMP cascade (like Leydig cells)

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what does does inner theca cell activation produce? via expression and activity of what?

produces androstenedione (androgen) via StAR activation

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what hormone stimulates granulosa cells? through what cascade?

FSH stimulates granulosa via cAMP cascade

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what 2 enzymes does FSH cause granulosa cells to produce?

aromatase and 17-beta-HSD

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what does aromatase convert androstenedione into? where does the androstenedione come from?

androstenedione (from neighboring theca cells) → estradiol via aromatase

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over time in granulosa cells, what happens to the amount of LH-receptors as FSH amounts increase? what is this process termed?

↑ FSH → ↑ LH receptors expressed; “luteinization”

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describe luteinization. what new hormone is produced? what is the granulosa cell called once luteinization occurs?

↑ FSH → ↑ estradiol → granulosa cells express LH receptors → progesterone prod.; “luteal cells”

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how does luteinization occur in granulosa cells for gene transcription of LH receptors to express?

ER receptors in granulosa cells start cascade

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what 2 proteins are produced upon presence of LH receptors and cAMP cascade? what are these required for?

StAR and 3-beta-HSD-II, which are needed for progesterone production

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prior to luteinization, why do granulosa cells not make much progesterone?

b/c don’t express genes for those enzymes/proteins

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what describes the switch from progesterone over estradiol production?

LH receptors > FSH receptors

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name and briefly describe the 2 menstrual cycle phases. how long do each last respectively? how long is a menstrual cycle in total?

  • follicular phase: tertiary follicle development until ovulation; 14 days long (day 1-14)

  • luteal phase: post-ovulation with formation and disintegration of corpus luteum; also 14 days long (day 14-28)

    • on average, menstrual cycle = 28 days long

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during ovulation (in the middle of menstrual cycle), what 2 hormones are both made? meanwhile, once oocyte leaves, which hormone is made more and why?

  • during ovulation: makes both progesterone and estradiol

  • after ovulation: LHR > FSHR → progesterone > estradiol prod.

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once corpus luteum is formed, what hormone keeps it going? how does the corpus luteum begin and continue disintegration?

LH keeps corpus luteum going, and continues to produce progesterone, until ↓ LH → corpus luteum disintegrates

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when in the menstrual cycle do estradiol levels rise? what causes this?

around day 10 in follicular phase; FSH stimulates granulosa cells to produce estradiol, continue cell division

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when in the menstrual cycle does LH levels experience a surge? what causes this?

around day 12/13 in follicular phase; ↑ GnRH pulse frequency → LH surge, with ↑ estradiol → pos. feedback @ AVPV nucleus → KISS neurons prod. KISS peptin → ↑ GnRH

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why are progesterone levels so low until day ~13?

progesterone note prod. as much until luteinization of granulosa cells, which express LH receptors and begin prod. ↑↑ progesterone; needs ↑↑ estradiol first

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why are progesterone levels drop around day ~25?

once oocyte leaves and follicle becomes corpus luteum, it only lives off of LH (which cont. progesterone prod.); however, LH starts ↓ and corpus luteum disintegrates → ↓ progesterone prod.

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name and briefly describe the 3 phases of the uterine cycle.

  1. menses: actual menstruation and sloughing off of endometrium

  2. proliferative phase: endometrium thickening

  3. secretory phase: maintaining of endometrium layer via progesterone effects

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for each phase of the uterine cycle, what is their corresponding day to the menstrual cycle?

  1. menses: day 1-7 (first half of follicular phase)

  2. proliferative phase: day 7-14 (second half of follicular phase)

  3. secretory phase: 14-28 (entire luteal phase)

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from the three, when do we see low estradiol levels?

  1. early follicular phase

  2. menstrual phase

  3. late luteal phase

all of these phases ft. low estradiol levels

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describe how increasing and further increase estradiol levels present a switch from high to low to high again levels of FSH and LH secretion.

  • initially: ↓ estradiol → ↑ FSH + LH via negative feedback in ARC

    • as ↑↑ estradiol → ↓ FSH + LH levels

  • then: ↑↑↑ estradiol → ↑ FSH + LH via positive feedback in AVPV

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locate on the menstrual cycle graph where ARC and AVPV compete for excitation.

  1. ARC neg. feedback and inhibition with ↑ estradiol (ft. drop)

  2. but, ↑↑ estradiol starts AVPV excitation

  3. → AVPV KISS neuron activation → ↑↑↑ pulse freq. for LH surge

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thus, at what levels does estradiol inhibit GnRH?

medium amounts of estradiol inhibit GnRH release

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describe estradiol regulation on AVPV vs. ARC in regards to KISS peptin release.

  • estradiol up-regulates expression of KISS peptin in AVPV; more peptin released

  • estradiol down-regulates KISS peptin in ARC; less peptin released

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as a rapid rise in LH induces ovulation, what appears at the edge of the ovary right before ovulation?

stigma, which is a pre-ovulatory follicle that ft. thinning of ovarian wall for exiting oocyte

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what 2 proteins are responsible for follicular and ovarian wall thinning?

plasmin and collagenase

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what is produced during pre-ovulatory gonadotrophin surge? what 2 things is it responsible for, which overall helps what?

  • prostaglandins, for expelling oocyte thru ovarian tube:

    • 1) contraction of smooth ovarian muscle

    • 2) constriction of local blood vessels

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what smooth muscle layer do prostaglandins stimulate? what does this do?

prostaglandins activate theca externa, which puts pressure on follicle to squeeze oocyte out

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how does the large quantities of luteal cells impact progesterone vs. estradiol production?

progesterone > estradiol prod.

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what type of cells are responsible for endometrium thickening?

stroma cells, which divide during proliferative phase

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why does endometrium thickening need to occur in the context embryo development? what hormone is responsible for thickening (stromal cell division)?

embryo embeds into endometrium stromal cells due to ↑ blood vessels presence, so endometrium is needed; thickening led by estradiol

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