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IMS: Physiology > Reproductive > Flashcards

Reproductive Flashcards

1
Q

Testes

A

Responsible for spermatogenesis and secretion of sex hormones.

  • Consists of two distinct anatomical and functional parts:
    1. Seminiferous tubules
      • encloses developing germ line
      • prevents indiscriminate exposure to plasma and interstitial fluid
    2. Endocrine cells
      • secrete sex steroid hormones, protein hormones, and other products for germ cell development
      • Sertoli cells ⇒ immediately surround germ cells
        • secrete mainly estrogens i.e. estradiol
        • secrete protein products
      • Leydig cells ⇒ more distant from germ cells
        • secrete maintly androgens i.e. testosterone
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2
Q

Ovaries

A

Responsible for spermatogenesis and secretion of sex hormones.

  • Consists of two distinct anatomical and functional parts:
    1. Follicle
      • encloses developing germ line
      • prevents indiscriminate exposure to plasma and interstitial fluid
    2. Endocrine cells
      • secrete sex steroid hormones, protein hormones, and other products for germ cell development
      • granulosa cells ⇒ immediately surround germ cells
        • secrete mainly estrogens i.e. estradiol
        • secrete protein products
      • Thecal (interstitial) cells ⇒ more distant from germ cells
        • secrete maintly androgens i.e. androstenedione
      • Luteal cells
        • transformed granulosae and theca cells
        • responsible for majority of progesterone secretion
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3
Q

Sex Hormone

Synthesis

A

Cholesterol is the precursor for androgens and estrogens.

Common pathway seen in both sexes.

Relative levels of a particular enzymes determines which steroids produced in given cell type.

  • 17-𝛼-hydroxylase
    • pregnenolone ⇒ progesterone
    • shunts production away from aldosterone and towards cortisol and androgens
    • under LH control
  • Aromatase
    • androstenedione ⇒ estrone
    • testosterone ⇒ estradiol
    • upregulation increases production of estrogens
    • under FSH control
  • 5-𝛼-reductase
    • testosterone ⇒ dihydrotestosterone (DHT)
      • DHT more potent androgen
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4
Q

Gonadotrophin-Releasing Hormone

(GnRH)

A

Produced by the hypothalamus and stored in the median eminence.

GnRH demonstrates pulsatile release.

Influenced by:

light-dark cycles via melatonin

stress hormones via CRH

olfactory stimulation via pheromones

Stimulates LH and FSH production/secretion from gonadotroph cells of anterior pituitary.

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5
Q

Hypothalamic-Pituitary-Gonadal Axis

(H-P-G)

A

H-P-G axis active during gestation, quiescent during childhood, and reactivates for puberty.

  • GnRH released from hypothalamus in pulsatile fashion.
    • GnRH stimulates both LH and FSH production/secretion from gonadotroph cells of anterior pituitary.
    • Which gonadotroph predominates depends on age and feedback mechanisms.
      • Low frequency GnRH release favors FSH.
      • High frequency GnRH release favors LH.
    • Prolonged stimulation by GnRH causes receptor downregulation and desensitization of gonadotrophs.
      • Results in inhibition of GnRH
      • Long-acting GnRH agonists therapeutically used for gonadotropin, androgen, and estrogen suppresion.
  • LH and FSH acts on gonads:
    • stimulates ovaries to produce progesterone and estradiol
    • stimulates testes to produce testosterone
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6
Q

H-P-G Axis

Regulation

A

Similar in males and females.

Occurs primarily through feedback loops:

  1. Testosterone and estradiol inhibits secretion of LH and FSH
  2. Inhibin reduces FHS synthesis and secretion
    • released from granulosa and Sertoli cells
  3. Activin stimulates FSH secretion
  4. Follistatin acts as activin-binding protein ⇒ prevents stimulation of FSH secretion by activin
    • acts as negative feedback
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7
Q

Two Cell - Two Gonadotropin

Theory

A

Actions of FSH and LH on two seperate cells to enable each cell to function.

  1. Sertoli & Leydig cells in males.
  2. Granulosa & thecal cells in females.
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8
Q

Sertoli Cells

A
  • Facilitates germ cell development in males
    • structural support and nutrition for germ cells
    • aids in spermiation
    • phagocytose residual bodies
  • Stop proliferating shortly after birth
  • Capacity to bind testosterone and FSH increases at puberty
  • FSH stimulates:
    • production of androgen-binding protein
      • storage protein for androgens in seminiferous tubules
      • androgen carrier from testis to epididymis
    • secretion of inhibin
      • negative feedback on FSH release by anterior pituitary
    • synthesis of aromatase
      • converts androgens into estrogens
  • Sertoli cells have nuclear androgen receptors but cannot produce testosterone.
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9
Q

Leydig Cells

A
  • Site of testosterone synthesis
  • Have LH receptors on surface
    • LH stimulates androgen secretion (mostly testosterone)
  • Have estradiol receptors but do not produce estradiol.
    • Estradiol can suppress response to LH.
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10
Q

Sertoli-Leydig

Interactions

A

Leydig cells and sertoli cells have bi-directional interactions.

  1. Leydig cells
    1. Have estradiol receptors but cannot produce it.
    2. Produces testosterone
      1. Testosterone diffuses to sertoli cells
      2. Allows high local androgen levels facilitating spermatogenesis
  2. Sertoli cells
    1. Have androgen receptors but cannot produce it.
    2. Converts testosterone ⇒ estradiol via aromatase.
      1. Estradiol diffuses to leydig cells
      2. Modulates Leydig response to LH
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11
Q

Thecal-Granulosa Cell

Interactions

A
  • Granulosa cells
    • Produces some progesterone in response to LH.
      • Cannot convert progesterone ⇒ androstenedione
    • Converts testosterone and androstenedione ⇒ estradiol via aromatase
      • Aromatase upregulated by FSH
      • Only granulosa cells have FSH receptors
    • Produces activin ⇒ stimulates FSH release
    • High levels of FSH stimulates inhibin release
      • Inhibin prevents actions of activin
      • Negative feedback decreases FSH release
  • Thecal Cells
    • Produces androstenedione and testosterone in response to LH
      • Androgens diffuse to granulosa cells
        • Converted to estradiol
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12
Q

Adrenarche

A

Adrenal Maturation

Precursor to centrally mediated puberty.

  • Zona reticularis gains ability to produce weak adrenal sex steroids
    • Dehydroepiandrosterone (DHEA)
    • Androstenedione
  • Results in some early signs associated with puberty e.g. sexual hair
  • Is not related to true H-P-G axis puberty
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13
Q

Puberty

(Gonadarche)

A

Transition from non-reproductive to reproductive stage.

Maturation of the H-P-G axis.

Depends on coordinated activity of hypothalamus, pituitary, and gonads.

  • Before age 10:
    • [LH and FSH]plasma low despite very low [gonadal hormones]
    • [FSH] > [LH]
  • Between age 9-17:
    • maturation of hypothalamic neurons
    • increased pituitary responsiveness to GnRH
    • pulsatile pattern of LH and FSH appears
    • ↑ GnRH pulse frequency ⇒ ↑ [LH]
    • noturnal peak in LH secretion seen during early and middle puberty
      • disappears as adult status reached
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14
Q

Adult

Gonadotropin Pattern

A

Once the adult pattern of gonadotrophin secretion established

Basal plasma [LH and FSH] similar between men and women.

[LH] > [FSH]

  • Women with dramatic monthly gonadotropin cycle
    • Related to menstrual cycle
    • LH bursts > FSH burts
  • Loss of gonadal responsiveness to gonadotropin stimulation ~ 5th decade in both sexes
    • Negative feedback ⇒ elevated gonadotropin levels
      • FSH > LH again
    • Change gradual in males
      • Some reproductive capacity till 9th decade
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15
Q

Sexual Differentiation

Types

A
  1. Genetic sex
    • set by chromosomes
      • XX = female
      • XY = male
  2. Gonadal sex
    • testes vs ovaries
  3. Genital Sex
    • phenotype of external genitalia
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16
Q

Male

Sexual Differentiation

A

At 5 weeks ⇒ indifferent stage

Gonads of ♂ and ♀ indistinguishable and genital tracts unformed.

Genetic sex determined by sex chromosomes.

At ~ 6 weeks ⇒ sexual differentiation begins

  • SRY gene on Y chromosome codes for testes determining factor (TDF)
    • Directs differentiation of primative gonad ⇒ testis
    • Directs multiple genes controlling genital tract differentiation
  • Androgen receptor on X chromosome
    • neccessary for maleness
    • sensitizes genital ducts and external genitalia to testosterone and DHT​
  • ♂ genital ducts and external genitalia differentiation requires specific hormones from ♂ gonad
    • Without such input female pattern results i.e. ♀ is default
  • Leydig cells ⇒ testosterone
    • causes Wolffian duct ⇒ vas deferens, seminal vesicles, ejaculatory ducts, further testis differentiation

At 9-10 weeks:

  • External genitalia begin to differentiate
  • ♂ phenotypic sex requires testosterone secretion and conversion to DHT by 5-𝛼-reductase
  • DHT ⇒ androgen receptor
    • Produce penis, scrotum, penile urethra, prostate
  • External genitalia differentiation complete by week 13 ⇒ start of phenotypic sex

Between 10-20 weeks:

  • Placental hCG predominant gonadotropin stimulating testosterone production.
  • Sertoli cells secrete anti-mullerian hormone (AMH)
    • Causes apoptosis of Mullerian ducts
17
Q

Female

Sexual Differentiation

A

At 5 weeks ⇒ indifferent stage

Gonads of ♂ and ♀ indistinguishable and genital tracts unformed.

Genetic sex determined by sex chromosomes.

At ~ 6 weeks ⇒ sexual differentiation begins

  • Requires both presence of X and absence of Y​
    • ♀ urogenital tract has adrogen receptors
    • No SRY/testosterone ⇒ Wolffian duct degeneration
    • No AMH ⇒ Mullerian duct persistance
  • Both X needed for ovary develpment
    • XO ⇒ Turner syndrome
      • normal female genitalia, abnormal streak gonads
  • Only one X needed for genital duct and external genitalia development

At 9-10 weeks:

  • External genitalia differentiation begins.
  • Clitoris, labia majora/minora, lower vagina develops unless masculinizing factors present
    • Controled by estradiol from ovaries
18
Q

Spermatogenesis

Environment

A
  • Begins at puberty within seminiferous tubules.
    • Testosterone required.
    • High levels of exogenous androgens produce infertility.
  • Blood-testis barrier formed by sertoli cells.
  • Seperates spermatogonia from descendents and external environment.
  • Testicular temperature 1-2°C below body temp.
  • Higher temperatures results in:
    • Slow mitosis and DNA production
    • Increase apoptosis of developing sperm
    • change in sperm morphology and motility
    • decrease inhibin production
      • raises FSH which decreases FSH receptors
19
Q

Spermatogenesis

Divisions

A

Spermatogonia (2N) undergo mitosis

Primary spermatocytes (2N) undergo meiosis I

Secondary spermatocytes (1N, 2 chromatids) undergo meiosis II

Forms spermatids (1N, 1 chromatid)

Become spermatozoa once released via spermiation.

20
Q

Spermatozoa Structure

A
  • Head
    • haploid nucleus with 23 chromosomes
    • acrosome
      • lysosome containing proteases used to penetrate ova
  • Midpiece
    • proximal part of tail
    • contains mitochondria which provides energy for the tail
  • Tail
    • flagellum consisting of 9+2 microtubule arrway
21
Q

Menstrual Cycle

A
  • ~ 2.5 million primary oocytes at birth
  • Declines to ~ 400,000 by onset of puberty
  • Oocytes frozen in meiotic prophase ⇒ primordial follicles
  • During menstraul cycle, small # of follicles mature
    • prepared for ovulation and potential fertilization
  • Cyclical changes of the ovarian cycle causes changes to the uterine cycle
  • Average length ~ 28 days
22
Q

Ovarian Cycle

Overview

A

Subdivided into 3 phases:

  1. Follicular phase (Estrogen driven)
    • Follicular growth due to FSH
    • Estrogen causes negative feedback
    • Dominant follicle selection occurs
    • Rising estrogen secreted by dominant follicle
    • High estrogen levels for 2 days switches HPO axis to positive feedback
    • Positive feedback causes mid-cycle LH surge > smaller FSH surge
    • LH surgce causes ovulation and luteinization of follicle
  2. Ovulation
    • LH weaknens the wall of the preovulatory follicle
  3. Luteal Phase (Progesterone driven)
    • Corpus luteum produces abundant progesterone and estrogen to lesser degeree.
    • high levels of progesterone causes negative feedback on HPO axis.
    • Corpus luteum has finite lifespan and degenerates
    • FSH/LH levels rise at the end due to loss of negative feedback
23
Q

Follicular Phase

Ovarian Cycle

A

Day 0-14.

Develops one follicle capable of ovulation and prepare uterus for actions of progesterone.

  1. Group of follicles enlarge through division of granulosa and thecal cells.
  2. By day 5-7, dominant follicle chosen.
    • May be related to # of FSH receptor & FSH sensitivity
  3. Dominant follicle produces highest [estrogen]
    • Abundant granulosa cells
    • Increased estrogen machinery
    • Estrogen with autocrine/paracrine affect
    • ↑ expression of estrogen and FSH receptors
    • sets up postitive feedback to ↑ estradiol synthesis
    • Antrum filled with follicular fluid and estrogen ⇒ creates microenvironment
    • promotes growth and steroid production
  4. Results in sharp rise of estradiol levels.
  5. Atresia of all but the dominant follicle occurs due to ↓ FSH
    • Granulosa cells produce inhibin ⇒ ↓ FSH
    • ↑ [estrogen] ⇒ desensitize gonadotrophs to GnRH ⇒ ↓ FSH
  6. Continued slow rise in [LH] despite GnRH inhibition
    • Estrogen alone unable to suppress tonic LH secretion
    • Both estrogen and progesterone required
24
Q

Control of Ovulation

A
  • High [estrogen]plasma
    • increases frequency of GnRH pulses by hypothalamus
      • ↑ both LH and FSH but favors LH release
    • targets LH secreting gonadotrophs in anterior pituitary to increase sensitivity to GnRH
  • When critical [estradiol]plasma sustained for 2 days
    • ​estrogen feedback on H-P-G axis from ⊖ ⇒ ⊕
    • results in LH surge
  • LH surge causes 4 major follicular changes:
    1. ⨂ estrogen synthesis by follicular cells
    2. ⨂ oocyte maturation inhibiting substance synthesis by granulosa cells ⇒ restarts oocyte meiosis
    3. Triggers prostaglandin production ⇒ induces ovulation via
      • vascular changes
      • follicular swelling
      • enzymatic digestion of follicular wall
    4. Differentiation of follicular cells ⇒ luteal cells
25
Q

Ovulation

Ovarian Cycle

A
  1. LH thins & weakens wall of pre-ovulatory follicle
    • via proteases, prostaglandins, and progesterone
  2. Wall rupture results in expulsion of secondary oocyte
    • ovulation occurs ~ 12 hours after LH surge
  3. Oocyte picked up by fimbria of oviducts
    • viable for possible fertilzation for ~ 24 hours
26
Q

Luteal Phase

A

Days 14-28.

Goal to increase progesterone levels and transform estrogen-primed uterus into evironment capable of nourishing an embyro.

  1. [LH] returns to baseline due to:
    • Dominant follicle demise ⇒ ↓ estrogen production
      • Steroid feedback on H-P-G axis switches from ⊕ to ⊖
    • Inhibin inhibition
  • LH stimulates corpus luteum secretion of progesterone ⋙ estrogen
    • Progesterone peaks ~ 7 days after LH surge
      • ~ 10x increase due to CL production
      • increases basal body temp set-point of hypothalamus by ~ 0.4 °C
    • Second estrogen peak occurs during luteal phase
      • Due to production by CL and pre-ovulatory follicles
      • Estrogen pattern described as biphasic
      • No associated LH surge d/t progesterone inhibition of LH & FSH
  • Luteolysis of CL begins due to ↓ LH ⇒ ↓ progesterone & estrogen
    • After 14 days degraded CL becomes corpus albicans scar
27
Q

Menses

Uterine Cycle

A

Cyclical changes in uterus due to ovarian hormone influences.

Day 1 of cycle = first day of menses.

  1. Menses
    • Starts at onset of ovarian follicular phase
    • Lasts ~ 4 days ± 2 days
    • Stratum functionalis shed
    • Due to ↓ [progesterone & estrogen] dueto CL demise
28
Q

Proliferative Phase

Uterine Cycle

A

Cyclical changes in uterus due to ovarian hormone influences.

  • Coincides with follicular phase of ovarian cycle
  • Stimulated by ↑ estrogen by developing follicles
  • Thickening of endometrial lining
    • due to proliferation epithelial & stromal cells
  • Insertion of estrogen receptors
    • perpetuation of estrogen action
  • Insertion of progesterone receptors
    • promotes endometrial responsiveness to progesterone
  • Elongation of spiral arteries
  • Cervical mucus: ↑ quantity, ↓ thickness
29
Q

Secretory Phase

Uterine Cycle

A

Cyclical changes in uterus due to ovarian hormone influences.

  • Uterus must be primed with estrogen before progesterone exposure for changes to occur
  • Coincides with luteal phase of ovarian cycle
  • Stimulated by progressive ↑ progesterone
  • Major effects of progesterone:
    • pro-implantation, pro-gestation
    • ⨂ epithelium proliferation via anti-estrogenic activity
    • differentiation of epithelial & stromal cells
    • production/secretion of glycogen-rich products from epithelial cells
    • predecidualization of stromal cells
    • ⨂ myometrial contractions
    • cervical mucus: ↓ quantity, ↑ thickness
30
Q

Progesterone’s

Anti-estrogenic Activity

A

Progesterone opposes the action of estrogen on the endometrium in 3 ways:

  1. inhibits synthesis of estrogen receptor
  2. decreases levels of estradiol by stimulating conversion to estrone
  3. inactivates estradiol through sulfation
31
Q

Menopause

A

The permanent cessation of menstruation and female reproductive function.

Defined as 12 months of amenorrhea.

Average age ~ 51.4 years.

  • Due to depletion of ovarian follicular pool
  • Menopause before age 40 considered premature ovarian failure
  • Usually involves period where menses irregular and anovulatory ⇒ menopause transition (perimenopause)
32
Q

Effects of Estrogen Loss

A
  1. Symptoms (early onset)
    • hot flashes/vasomotor symptoms
    • minor mood disturbances
    • sleep disturbances
    • urogenital symptoms
  2. Physical signs (intermediate onset)
    • vaginal atrophy
    • osteopenia
    • scalp hair loss or hirsutism
  3. Potential Diseases (Later Onset)
    • osteoporosis
33
Q

Fertilization

A

For successful fertilization, fresh sperm must be present when ovum enters the oviduct.

Sperm and ovum degenerates within ~ 24 hours of release.

  1. Sperm moves through follicular cells to attach to zona pellucida.
    • Receptor on sperm head ⇒ ZP3 in zona pellucida ⇒ transduction cascade within sperm head
  2. Cascade induces acrosomal reaction.
    • Proteolytic enzymes released from acrosome
    • Dissolves zona pellucida allowing sperm entry
    • Penetrates via proteolysis combined with mechanical motion.
  3. Sperm and egg membranes fuse ⇒ cytoplasmic contents of sperm enter egg
  4. Sperm head penetrates egg membrane ⇒ signal transduction cascade ⇒ oscillatory ↑ in cytoplasmic [Ca2+].
  5. ↑ cytoplasmic [Ca2+] ⇒ 2nd meiotic division of egg & cortical reaction
    • Causes zona pellucida to harden and prevent polyspermy
  6. Meiosis II completed forming second polar body.
    • Both polar bodies secreted into space between egg membrane and vitelline membrane.
  7. Chromosome of egg decondenses ⇒ female pronucleus.
  8. Sperm nucleus decondenses ⇒ male pronucleus
  9. Male & female pronuclei fuse ⇒ zygote ⇒ end of fertilization
34
Q

Implantation

A
  1. Fertilization occurs.
  2. Serial divisions occur as zygote travels down fallopian tube producing blastocyst.
  3. Blastocyst implants itself into uterine wall.
    • Takes 7 days.
    • Uterus must be primed by estrogen & progesterone.
    • Endometrium must have undergone decidualization.
  4. Outer layer of cells in blastocyst forms trophoblast.
  5. Trophoblasts release proteases permiting endometrial invasion by blastocyst.
  6. Blastocyst secretes immunosuppressive agents and hCG to ensure its survival.
    • hCG mimics actions of LH and sustains corpus luteum.
  7. When implantation successful, series of divisions and differentiations forms placenta.
    • Syncytiobalst lacunae fuse forming maternal blood space.
    • Embryo chorionic villi invade spaces connecting fetal and maternal blood.
35
Q

Placenta

Functions

A
  1. anchors fetus to uterus
  2. brings maternal and fetal blood in close apposition and facilitates exchange
  3. endocrine organ that maintains pregnancy
36
Q

Placental Structure

A

Two parts: maternal placenta and fetal placenta.

  • Fetal placenta attached to fetus via umbilical cord
    • 2 umbilical arteries
      • O2 poor blood from fetus ⇒ chorionic villi
    • 1 umbilical vein
      • O2 rich blood from villi ⇒ fetus
  • O2 rich blood from mother enters maternal placenta via spiral arteries
    • Opens into intervillous space bathing chorionic villi
    • No capillaries in maternal placenta
    • Pool leaves via venal orifices that connect with uterine veins
  • Fetal and maternal circulations physically distinct and do not intermix normally.
    • Most material crosses via simple diffusion
    • Process enchanced by large SA of chorionic villi on fetal side and microvilli on maternal side
37
Q

Placenta

Endocrine Functions

A

Fetal placenta produces endocrine mediators that alters the mother’s reproductive physiology in order to sustain pregnancy.

  1. Human chorionic gonadotropin (hCG)
    • secreted by syncitiotrophoblasts
    • sustains progesterone and estrogen production by corpus luteum
    • basis for UPTs
  2. Progesterone
    • secreted by syncitiotrophoblasts
    • prepares endometrium for implantation
    • prevents uterine contractions that might dislodge embryo
  3. Estrogens (mainly estriol)
    • stimulate growth and development of mother’s uterus and breasts
    • production involves the placenta, fetus, and mother
38
Q

Embryonic

Steroid Hormone Production

A

Involves complex interchange of materials between mother, placenta, and fetus.

  • Placenta
    • Has minimal supply of cholesterol
    • Does not possess 17-𝛼-hydroxylase
  • Fetal adrenal cortex
  • Maternal compartment

IMS: Physiology (14 decks)

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