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Endocrinology Final > Reproductive Endocrinology > Flashcards

Reproductive Endocrinology Flashcards

1
Q

Explain the synthesis of sex hormones.

A
  1. Cholesterol
  2. Pregnenolone -> Progesterone
  3. Other steps
  4. Androstenedione -> estrone (CYP19) and testosterone (17beta-HSD)
  5. Testosterone -> estradiol (Aromatase/ CYP19)
  6. Testosterone -> Dihydrotestosterone (5alpha-reductase)
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2
Q

Carnegie Stages

A

System used by embryologists to describe the apparent maturity of embryos (Embryonic, E)

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3
Q

Postovulatory Age

A
  • Frequently used by clinicians to describe the maturity of an embryo
  • Refers to the length of time since the last ovulation before pregnancy (days, d)
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4
Q

Gonadal Ridge

A
  • Bipotential gonad
  • First thing to differentiate
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5
Q

Rspo1

A
  • XX
  • Wnt4/beta-catenin
  • Female gene development: Mullerian duct (uterine tube)
  • Reduction of Wolffian duct
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6
Q

Sry

A
  • XY
  • Sox9
  • Testosterone and Anti Mullerian hormone (AMH)
  • AMH represses female gonadal development
  • Wolffian duct development (vas deferens)
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7
Q

What are the components of male genitalia?

A
  • 2 testes
  • 2 ductus deferens
  • Accessory sex glands (prostate, seminal vesicles, etc.)
  • Pelvic/penile urethra
  • Penis
  • Seminal vesicle is testosterone tissue
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8
Q

What are the components of female genitalia?

A
  • 2 ovaries
  • 2 uterine tube/oviduct
  • Uterus
  • Cervix
  • Vagina
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9
Q

Explain the process of sexual differentiation of the brain.

A
  • Androgens produced by fetal and neonatal testes are converted to estradiol in the brain by aromatase
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10
Q

Bovine Twins

A
  • Female (XX): does not have reproductive anatomy (infertile)
  • Freemartin
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11
Q

Dichlorodiphenyltrichloroethane (DDT)

A
  • Androgen receptor antagonist (DDE) (can also bind to estrogen receptor beta) -> not activated (poor or no differentiation in tissues)
  • Endocrine disruptor
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12
Q

Explain the HPG axis basics.

A
  1. Hypothalamus: Gonadotropin releasing hormone (GnRH)
  2. Anterior Pituitary Gland: Luteinizing Hormone/ Follicle Stimulating Hormone (LH/FSH)
  3. LH -> endocrine cells -> steroid and peptide hormones
  4. FSH -> gamete production
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13
Q

Oxytocin

A
  • Effects: milk ejection, uterine smooth muscle contraction, maternal behavior
  • Positive control: physical stimulation (teat/nipple/cervical) and psychological (visual/auditory)
  • Negative control: catecholamines (stress)
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14
Q

Explain GnRH neuron input.

A
  • Kisspeptin neuron -> GnRH neuron (releases GnRH)
  • GnRH neurons do not express steroid R
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15
Q

Inhibin

A
  • Blocks FSH production
  • Androgens stimulate inhibin
  • Gonadal inhibin: decreases FSH production by blocking action of activins
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16
Q

Activin

A
  • Supports LH (activin A) or FSH (activin B) production
  • Follistatin binds to activin and prevents it from increasing FSH
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17
Q

Explain the male HPG axis.

A
  1. Hypothalamus: secretes GnRH
  2. GnRH in hypothalamo-pituitary portal vessels
  3. Anterior pituitary: secretes FSH and LH
  4. FSH -> Sertoli cells in testes -> stimulate spermatogenesis and inhibin
  5. LH -> Leydig cells -> testosterone -> Reproductive tract and other organs
  6. Inhibin -> negative feedback to anterior pituitary (only FSH)
  7. Testosterone -> negative feedback to hypothalamus and anterior pituitary (only LH)
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18
Q

Explain the female HPG axis.

A
  1. Hypothalamus: secretes GnRH
  2. GnRH in hypothalamo-pituitary portal vessels
  3. Anterior pituitary: secretes FSH and LH
  4. FSH -> Granulosa cells in ovaries -> influence oocytes, secrete inhibin, and convert androgens to estrogen
  5. LH -> Theca cells -> androgens
  6. Inhibin -> negative feedback to anterior pituitary (primarily FSH)
  7. Estrogen -> positive feedback to anterior pituitary and hypothalamus
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19
Q

Where is testosterone produced in males?

A

Interstitial space (Leydig cells)

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20
Q

What types of cells are found in the seminiferous tubules?

A
  1. Germ cells (spermatogonia)
  2. Sustentacular (Sertoli cells): produce inhibin
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21
Q

Leydig Cells

A
  • Interstitial space (between seminiferous tubules)
  • Respond to LH to secrete testosterone (feedback to brain to decrease GnRH and LH
  • Indirectly support spermatogenesis by producing testosterone
  • Rich in steroidogenic enzymes necessary for steroidogenesis (testosterone production)
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22
Q

Sertoli Cells

A
  • Support germ cells
  • Secrete inhibins (feedback to brain to decrease FSH)
  • Respond to FSH
  • In fetal life, secrete AMH
  • Form tight junctions (blood testis barrier)
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23
Q

What are the roles of testosterone?

A
  • Stimulate spermatogenesis
  • Maintain Wolffian duct, accessory glands
  • External genitalia, secondary sex characteristics
  • Simulate metabolism (muscle growth)
  • Affect CNS function/behavior
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24
Q

Cryptorchidism

A
  • Undescended testes
  • Most common birth defect of male genitalia
  • Will not produce normal sperm but will produce androgens
  • Increased risk of testicular cancer
  • Caused by hormonal abnormalities, genetic or environmental changes
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25
Q

Kisspeptin

A
  • Receptor: KISS1R/ GPR54 (Gq, PLC)
  • Produced by neurons and adipose tissue (increased with obesity)
  • Inactivating mutations of KISS1R/GPR54 or KP leads to reproductive failure (hypogonadotropic hypogonadism)
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26
Q

Gonadotropin Inhibiting Hormone (GnIH)

A
  • GnIH-R (GPCR) found on GnRH neurons and gonadotropes
  • Inhibits reproductive axis, counterbalancing GnRH1 (primary form of GnRH that stimulates gonadotropin release)
  • Responsive to environmental factors (stress and photoperiod)
  • Increased when reproduction is less advantageous
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27
Q

Explain the four stages of puberty.

A
  1. Prepubertal stage: growth and development determined by nutritional status, genetics, and environmental factors, GnRH suppression: GnRH is low (LH/FSH suppressed)
  2. Pubertal Onset: Hormonal activation (GnRH pulses increase in frequency and amplitude, stimulating the anterior pituitary to release FSH and LH) and follicle and seminiferous development (FSH stimulates follicle development in the ovaries, spermatogenesis in the testes)
  3. Sexual Maturation: secondary sexual characteristics (increased levels of sex steroids lead to visible secondary sexual characteristics, such as muscle growth and behaviors) and first ovulation or spermatogenesis (production of viable sperm in males and first ovulation in females males functional reproductive maturity)
  4. Reproductive capability: regular cyclicity in females (females begin regular estrous cycles) and sperm maturation in males (sperm production sufficient to support fertility over time)
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28
Q

Tanner Staging (Sexual Maturity Rating)

A
  • Used by human healthcare providers to document and track the development of secondary sex characteristics of children during puberty

Stage 1: Hormone are active, but no visible signs of puberty
Stage 2: first physical signs of puberty appear (breast buds or pubic hair)
Stage 3: Growth spurt, acne, axilla hair growth
Stage 4: Development continues and first menses occurs in females
Stage 5: Reproductive organs and genitals are fully developed and facial hair appears in males

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29
Q

What are the signals for pubertal onset?

A
  1. Age: nutrition, genetics, body condition or critical body weight by a certain age
  2. Timing: season/photoperiod, social cues, pheromones
  3. Endocrine input/disruption: GnRH, leptin (body condition), Kisspeptin (key signaling mechanism from adipose tissue), GnIH
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30
Q

How is prostaglandin synthesized?

A
  1. Plasma membrane with membrane bound phospholipids
  2. Stimulus activates phospholipase
  3. Arachadonic acid
  4. Cyclooxygenase (COX)
  5. Eicosanoids (ex: prostaglandin F2 alpha in uterus)
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31
Q

Anti-Mullerian Hormone (AMH)

A
  • Protein hormone
  • AMH-receptor 2 (TGFbeta type)
  • Produced by Sertoli cells of the testes of XY fetus during sexual differentiation
  • Causes Mullerian ducts (precursors to female reproductive organs) to regress and may help with testicular descent
  • Produced by granulosa cells of ovary of XX fetus after Mullerian ducts have regressed
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32
Q

Granulosa cells

A
  • Secrete inhibin in response to FSH
  • Produce estrogen under influence of FSH and LH
  • Convert androgens to estrogens
  • Have FSH receptor
33
Q

Explain the HPG axis in the late follicular phase, early luteal phase.

A
  1. Estrus (ovary) -> large amounts of estrogen
  2. Positive feedback to hypothalamus and anterior pituitary
  3. Hypothalamus: secretes GnRH
  4. GnRH in hypothalamo-pituitary portal vessels
  5. Anterior pituitary: secretes LH
  6. LH surge -> diestrus (progesterone and estrogen)
34
Q

Explain the HPG axis in the luteal phase (diestrus).

A
  1. Diestrus (corpus luteum) -> inhibin and progesterone and estrogen (PGF2alpha removed CL)
  2. Inhibin -> negative feedback to anterior pituitary (primarily FSH)
  3. Progesterone and estrogen -> negative feedback to hypothalamus and anterior pituitary
  4. Hypothalamus: decreased secretion of GnRH
  5. GnRH in hypothalamo-pituitary portal vessels
  6. Anterior pituitary: secretes FSH and LH (decreased)
35
Q

Explain the development of a corpus luteum.

A
  1. Cohort of follicles (ovaries) (amount of follicles is dependent on the amount of estradiol)
  2. FSH grows follicles (follicles have FSHR)
  3. Follicles will produce some estradiol
  4. Dominant follicle: follicle with increased estradiol production, LH-R, and inhibin production
    (Non-dominant follicles undergo atresia (die off))
  5. Inhibin produced from dominant follicle -> inhibits FSH -> blocks rest of cohort from developing
  6. LH surge -> luteinization -> corpus luteum (increased progesterone)
36
Q

Estrus Phase

A
  • Estrogen dominant
  • Animal is sexually receptive
  • Includes day of ovulation (ovulation leads to formation of corpus luteum)
  • LH surge (immediately after ovulation due to large estrogen amounts)
  • Follicular phase
37
Q

Proestrus

A
  • Preparatory stage for estrus (animal is coming into heat)
  • Characterized by the transition from progesterone dominance to estrogen dominance
38
Q

Metestrus

A

Brief period when the endocrine milieu shifts from estrogen dominance to progesterone dominance

39
Q

Diestrus

A
  • Progesterone dominant
  • Waiting to recognize pregnancy
  • Luteal phase
  • FSH waves
  • PGF2alpha: not pregnant -> progesterone decreases -> gets rid of corpus luteum
40
Q

Anestrus

A

No ovarian activity occurring

41
Q

What happens in the follicular phase?

A
  • FSH stimulates follicle growth
  • Estrogen levels are low (little negative feedback)
  • Growing follicles secrete little estrogen
  • Dominant follicle (LH-R) secretes large amounts of estrogen and inhibin
  • High levels of estrogen cause LH surge (completion meiosis I)
  • Increase in vaginal secretions
  • Opening/softening cervix
42
Q

What happens in the luteal phase?

A
  • Ovulation occurs -> formation of corpus luteum
  • Corpus luteum secretes large amount of estrogen and progesterone
  • Negative feedback to brain -> FSH and LH levels drop
  • Corpus luteum degenerates, estrogen and progesterone levels drop
  • FSH and LH start to increase again -> new cycle
  • Decrease in vaginal secretions
  • Closing of cervix
  • Production of mucus to cover cervix
  • Secretion of “uterine milk” for embryo
43
Q

What influences the endometrium in a cyclic manner?

A

Rise and fall of estrogens and progesterone

44
Q

What are the major functions of estrogen (estradiol)?

A

Follicle growth, development of secondary sex characteristics, growth and proliferation epithelial lining of reproductive tract, feedback to brain, inhibits milk production, facilitates estrus behavior

45
Q

What are the major functions of progesterone?

A

Preparation of the endometrium for embryo implantation, stimulates breast growth, negative feedback to brain, inhibits milk production, inhibits myometrial contractions, facilitates diestrus behavior and progestation

46
Q

Lordosis

A
  • Standing heat
  • Estrogen
  • Testosterone, progesterone also can impact sex drive
  • Clitoral enlargement, demonstration
47
Q

What are the three control mechanisms for ejaculation?

A
  1. Endocrine regulation: oxytocin, prolactin/thyroid hormones, estrogens/testosterone, glucocorticoids / serotonin/dopamine /norepinephrine
  2. Chemical regulation: parasympathetic primes and sympathetic fires
  3. Electrical ejaculation
48
Q

Intratubal Insemination (ITI)

A

Sperm is deposited at the uterine tubal junction

49
Q

Intrauterine insemination (IUI)

A

Sperm is deposited directly into the uterus

50
Q

Intracervical insemination (ICI)

A

Sperm is deposited at the cervix

51
Q

Vaginal Insemination

A

Sperm is deposited into the vagina

52
Q

In vitro fertilization (IVF)

A

Method of insemination that involves other procedures

53
Q

Explain the role of estrogen in sperm transport and readiness.

A
  • Increases uterine and vaginal secretions (facilitate sperm movement)
  • Increase uterine muscle contractions (help transport sperm)
54
Q

Explain the role of sperm capacitation in sperm transport and readiness.

A
  • Before fertilizing an egg, sperm undergo process called capacitation in female reproductive tract
  • Influenced by hormones and tract secretions
  • Removes certain proteins and enhances sperm motility -> makes sperm capable of binding to and penetrating egg
55
Q

Explain the role of the acrosome reaction in sperm transport and readiness.

A
  • Acrosome reaction triggered by contact with the egg’s outer layer (zona pellucida)
  • Involves enzymes released from the sperm’s acrosome cap to help penetrate the zona and reach the egg’s plasma membrane for fertilization
56
Q

Assisted Reproductive Techniques (ART)

A
  • Ovum pickup (OPU)
  • In vitro fertilization (IVF)
  • Intracytoplasmic sperm
57
Q

PGE2

A
  • Responsible for early embryo transport out of the oviduct into the uterus
  • Fatty acid (GPCRs)
58
Q

Antiluteolytic

A
  • Save the CL helps to prevent CL demise
  • IFNT (ruminant) and estradiol/Prl (sow)
59
Q

Luteotropic

A
  • Helps CL grow (increasing CL progesterone production)
  • CGbeta (primates) and Prl (rodents)
60
Q

Human Chorionic Gonadotropin (hCG)

A
  • Necessary for maintaining the CL in women by directly supporting CL progesterone production
  • Acting like and LH receptor agonist
  • Luteotropic
  • Can be used to induce ovulation in female
61
Q

Explain gonadotropin structure (alpha and beta subunits).

A
  • All gonadotropins are made up on alpha and beta subunit
  • Share alpha subunit with TSH and the chorionic gonadotropin produced by placenta
  • Receptor specificity determined by beta subunit (hCG binds to LH receptor)
62
Q

Placentation

A
  • Continuous endocrine process
  • Begins with blastocyst (trophoblast)
  • Fetal adrenal glands (end)
63
Q

Case Study: A dairy producer would like to improve the farm’s reproductive efficiency through the use of ART. What are some of the options and how might they benefit the herd?

A
  • Begin: valuable donor and crossbred recipients (estrous synchronization: PGF2alpha)
  • Valuable donor -> superovulation (FSH given to increase cohort and growth) (FSH can override inhibin to continue growth)
  • Valuable sire -> insemination at estrus (GnRHR or LHR agonist)
  • Embryo recovery: PGF2alpha (in case all embryos are not transferred)
  • Crossbred recipients -> estrus (GnRH or LHR agonist): donor and recipient lined up at time of ovulation
  • Progesterone to get valuable offspring
64
Q

Sperm Sexing

A
  • Sort sperm using DNA content differences
  • Y and X chromosomes appear different with laser
  • 99% efficiency
  • Process decreases viability of sperm
65
Q

What are the six key hormones in human pregnancy?

A
  1. Human Chorionic Gonadotropin (hCG): produced by placenta after implantation; supports function of CL
  2. Progesterone: helps establish placenta; stimulates growth of blood vessels and inhibits contractions (smooth muscle relaxation)
  3. Estrogen: helps uterus growth (maintains lining)
  4. Prolactin: breast milk production, enlargement of mammary glands
  5. Relaxin: inhibits uterus contraction to prevent premature birth
  6. Oxytocin: facilitates delivery (rises at labor) by stimulating contractions of uterine muscle; triggers production of prostaglandins
66
Q

How does fetal cortisol impacts parturition (labor)?

A
  • Towards the end of pregnancy, fetal adrenal glands begin producing cortisol
  • Helps mature fetal organs (lungs) and signals to the placenta to increase estrogen production -> prepare for labor
67
Q

How does the estrogen to progesterone ratio shift impact parturition (labor)?

A
  • Increase in estrogen relative to progesterone promotes uterine contractions, helping initiate labor
  • Estrogen also increases oxytocin receptors on uterus (makes it more responsive to oxytocin)
68
Q

How does oxytocin and prostaglandins impact parturition (labor)?

A
  • Oxytocin from maternal pituitary and prostaglandins from uterus work together to stimulate strong uterine contractions that drive labor
  • Oxytocin also enhances bonding after birth and triggers milk ejection during breastfeeding
69
Q

Explain the three stages of labor.

A
  1. Cervix relaxes, causing it dilate and thin out
  2. Uterine contractions increase in strength and the infant is delivered
  3. Placenta is expelled (oxytocin)
70
Q

Explain the differences between mammogenesis, lactogenesis, and galactopoiesis.

A
  1. Mammogenesis: mammary tissue development (during pregnancy)
  2. Lactogenesis: start of lactation (parturition)
  3. Galactopoiesis: Production of milk (lactation)
71
Q

Prolactin

A
  • Produced by lactotrophs of the anterior pituitary gland during pregnancy
  • Responsible for milk production and breast development
  • Levels controlled by other hormones (inhibited by dopamine)
  • Protein hormone
  • Effects: induces lobuloalveolar growth of mammary gland, stimulates lactogenesis, along with cortisol and insulin, acts to stimulate transcription of genes that encode milk proteins
72
Q

Placental Lactogen

A
  • Produced by placenta during pregnancy
  • Prepares body for breastfeeding and regulates metabolism
  • Ensures fetus receives enough nutrients
73
Q

Brain-Breast- Bone Circuit

A
  • Breast is central regulator of skeletal demineralization during lactation to make calcium and other minerals for milk production
  • Suckling and prolactin inhibit GnRH pulse center -> suppress LH and FSH -> low levels of estradiol and progesterone
  • Parathyroid hormone related protein (PTHrP) production and release from breast controlled by suckling, prolactin, and calcium receptor
  • PTHrP enters bloodstream (with low estradiol levels) -> upregulate bone resorption -> releases calcium and phosphate into blood -> breast milk
74
Q

The CL actively secretions which hormone?

A

Estrogen and progesterone

75
Q

Which of the following would occur after removing the testicles of a dog?

A

Increase in LH (due to increase in GnRH)

76
Q

Explain the HPG axis during female menopause.

A
  1. Decreased estrogen production and release in granulosa cells
  2. Positive feedback to hypothalamus -> increased GnRH
  3. Increased LH and FSH
77
Q

Explain the HPG axis during the follicular phase.

A
  1. KP -> KISS1R/GPR54 -> GnRH
  2. FSH, LH
  3. LH -> estrogen
  4. FSH -> follicular recruitment (follicles have FSHR) -> dominant follicle (LHR, increased estrogen, inhibin)
  5. Inhibin -> other follicles (atresia) and inhibits FSH
  6. Dominant follicle ovulates with granulosa cells
  • hCG mimics LH surge
78
Q

Explain the HPG axis in male puberty.

A
  1. Adipose -> KP (leptin increases KP) -> GnRH
  2. Increased GnRH
  3. Increased LH
  4. Increase in androgens in Leydig cells (Nurse) -> increase testosterone
  5. Testosterone -> Sertoli (Secretory cells) cells -> increase spermatogenesis
  6. Increased testosterone -> negative feedback to hypothalamus and pituitary
  7. Sertoli cells -> inhibin -> inhibit LH
  • GnIH inhibits GnRH

Endocrinology Final (13 decks)

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