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Reproduction Flashcards

0
Q

What will occur with gonadal development if someone is XO?

A

Ovarian (gonadal) streaks.

Ducting and external genitalia will be normal female.

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1
Q

What portion of the Y chromosome determines sex?

A

SRY

Makes TDF (testis0determining factor)

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2
Q

What stage are primary oocytes in?

A

Diplotene stage

Part of prophase.

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3
Q

How many daughter cells are produced per germ cell in spermatogenesis?
Oogenesis?

A 
Spermatogenesis = 4
Oogenesis = 1 and polar bodies
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4
Q

What does the Coelomic Epithelium develop into?

A

Sertoli cells in XY male
Granulosa cells in XX female

Sertoli cells release antimullerian hormone

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5
Q

What do mesenchymal cells develop into?

A

XY: Leydig cells
XX: Theca cells

Leydig cells –> androgens
Theca cells –> E2

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6
Q

What determines gonadal development?

A

It is genetically determined & hormone-independent.

This makes sense since the gonads are the source of sex hormones.

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7
Q

What does the gonadal medulla develop into?

The cortex?

A

Medulla = seminiferous tubules, spermatogonia, sertoli, leydig

Cortex: Secondary sex cords, oogonia, theca, granulosa

Medulla results from XY, Cortex results from XX.

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8
Q

What do Sertoli cells secrete?

A

Antimullerian hormone

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9
Q

What do Leydig cells secrete?

A

Testosterone

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10
Q

What do Theca cells secrete?

A

E2

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11
Q

What is testosterone’s effect on duct development?

A

Testosterone keeps Wolffian ducts around

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12
Q

What is Antimullerian hormone’s (AMH’s) effects on ductal development?

A

It regresses Müllerian ducts.

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13
Q

What enzyme catalyzes Testosterone –> DHT?

A

5-alpha-reductase

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14
Q

What drug blocks 5-alpha-reductase?

A

Propecia

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15
Q

Turner’s Syndrome:
Genetics?
Gonads?
External genitalia?

A

XO

Streak gonads

Female external genitalia

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16
Q

What determines female/male pseudohermaphroditism?

A

If testes are present –> male pseudo…

If both types of gonads present –> hermaphroditism

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17
Q

Androgen Resistance:
Genetics?
Gonads?
Exterior appearance?

A

Genetics: XY; X-linked androgen receptor is messed up.

Internal testis present

Looks like female; no axillary/pubic hair present.

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18
Q

Klinefelter’s Syndrome:
Genetics?
Symptoms?

A

XXY

Infertile; uppter:lower segment is off; short arms; gynecomastia; triangle pubic hair.

This is the most common form of primary testicular failure.

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19
Q

Kallmann’s Syndrome:
Symptoms?
Cause?

A

Symptoms: anosmia, microphallus

Cause: GnRH neurons can’t get into CNS (congenital)

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20
Q

Female Pseudohermaphroditism:
Cause?
Symptoms?

A

Cause = prenatal exposure to androgens

Symptoms: clitoromegaly, possible urogenital sinus, advanced skeletal age.

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21
Q

Where do spermatagonia travel as they develop into spermatids?

A

Inward toward the lumen of a seminiferous tubule.

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22
Q

What catalyzes Testosterone —> E2?

A

Aromatase

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23
Q

What is spermiogenesis?
Spermatogenesis?
Spermeation?

A

Spermiogenesis = maturation & remodeling of sperm

Spermatogenesis = Spermiogenesis + Spermeation

Spermeation = Extrusion of flagellated spermatozoa into lumen of seminiferous tubule and removal of remaining cytoplasm as residual body.

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24
Q

When do sperm become haploid?

A

During the second meiotic division.

Secondary spermatocyte —-> Spermatid

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25
Q

What is the acrosome?

A

Membranous cap filled with digestive enzymes.

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26
Q

What forms the blood/testis barrier?

A

Tight junctions between Sertoli cells keep Ig’s away from developing sperm.

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27
Q

What function does the epididymis serve?

A

It is a reservoir for sperm and allows their maturation.

Sperm gain motility and lose their cytoplasm while being stored.

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28
Q

What purpose does the prostate gland serve?

A

It secretes alkaline additives to the semen. This helps to neutralize the acidic vagina.

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29
Q

What does PSA measure?

A

Prostate-Specific Antigen.

It is used as a clinical indicator of prostate hyperplasia and prostate cancer.

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30
Q

What purpose do the seminal vesicles serve?

A

They secrete prostaglandins, which cause uterine and Fallopian tube contraction. This facilitates sperm movement.

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31
Q

How is LH regulated?

A

GnRH stimulates it.

Testosterone is converted to estrogen in the hypothalamus and feedback inhibits GnRH release.

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32
Q

What is the major regulator of FSH?

A

Inhibin

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33
Q

What occurs in Leydig cells, in response to LH?

A

LH –> GPCR –> PKA –> transcription.

Testosterone is produced, as well as sterol-carrier protein & sterol-activating protein.

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34
Q

What occurs in Sertoli cells in response to FSH?

A

FSH –> GPCR –> PK –> transcription.

^Androgen Receptors
^Aromatase
^Growth factors for spermatogenesis
^Inhibin synthesis

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35
Q

What cells release inhibin/activin?
What is their endocrine action?
What is their paracrine action?

A

Sertoli cells release them.

They work like their namesake when influencing the pituitary (endocrine), but they work OPPOSITE of their namesake when influencing Leydig cells (paracrine).

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36
Q

What is the effect of Testosterone on Sertoli cells?

A

It stimulates them indirectly, this is mediated by stimulating Peritubular Myoid cells, which stimulate Sertoli cells.

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37
Q

What are the paracrine inhibitors of Leydig cells?

A

Activin & E2

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38
Q

How do germ cells regulate their own levels?

A

They release signals that cause inhibin release from Sertoli cells.

If there are many dividing germ cells –> inhibin release –> decreased FSH –> levels return to normal

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39
Q

What is the most common cause of male infertility?

A

It is most commonly idiopathic.

40
Q

What is the cumulus oophorus?

A

The granulosa cells that directly surround the oocyte within a follicle.

41
Q

What is the corona radiata?

A

It is the portion of cumulus oophorus that is directly adjacent to the Zona Pelucida within a Graafian follicle.

42
Q

What type of follicle are most?

A

Primordial follicles = 90-95% of follicles

43
Q

When do follicular cells differentiate into Granulosa cells?

A

During the Primary Follicular stage

44
Q

What is the Zona Pellucida?

What forms it?

A

It is a polysaccharie coat around the oocyte. It is formed by granulosa cells.

45
Q

What causes the increase in osmotic pressure seen in the Graafian follicle?

A

Depolymerization of mucopolysaccharides.

46
Q

What does Follistatin do?

A

Neutralizes Activin.

47
Q

Where is Inhibin A made?

Inhibin B?

A

Inhibin A: Corpus Luteum

Inhibin B: Dominant Follicle

48
Q

What produces inhibin in the female?

A

Granulosa cells.

49
Q

What is activin composed of?

Inhibin?

A 
Activin = 2 beta subunits
Inhibin = 1 alpha, 1 beta subunit
50
Q

When is a secondary oocyte formed?

A

Upon ovulation, when the first meiotic division finishes.

51
Q

What happens to Theca and Granulosa cells following ovulation?

A

They undergo Leutinization:

Differentiation
Hypertrophy
Lipid droplets

52
Q

What happens to the corpus luteum if no fertilization occurs?

A

Luteolysis = regression of CL

Corpus luteum –> corpus albicans

53
Q

How is hypothalamic secretion of GnRH regulated?

A

Dopamine inhibits
Endorphins inhibit
Test/E2 inhibit

NE activates

54
Q

What is the rate-limiting step in steroid biosynthesis in females?

A

Desmolase

55
Q

What are the major progestins?

A

Progesterone

17alpha-hydroxyprogesterone

56
Q

How are estrogens transported in the blood?

Progesterone?

A

Estrogens = albumin & SHBG

Progesterone = albumin & CBG

Both are mostly bound to albumin.

57
Q

Within gonadotrophs, what causes increased FSH/LH transcription?

A
  1. GnRH binds GnRH-R
  2. G-alpha-q activated
  3. PLC activated (generates DAG & IP3)
  4. DAG activates PKC
  5. PKC changes gene expression –> activates FSH/LH transcription
58
Q

Within gonadotrophs, how is FSH/LH secretion regulated?

A
  1. GnRH binds GnRH-R
  2. G-alpha-q activated
  3. PLC activated (generates DAG & IP3)
  4. IP3 binds to IP3-R on endoplasmic reticulum
  5. Ca2+ release from ER –> vesicle fusion & exocytosis
59
Q

What does FSH do broadly in females?

A

It facilitates follicular development and E2 secretion.

60
Q

What does LH do broadly in females?

A

It promotes ovulation and leutinization.

61
Q

Where in the ovary do estrogens come from?

Progestins?

A

Estrogens: Follicle
Progestins: Corpus Luteum

62
Q

Where are androgens produced in the female?

Are they direct testosterone or peripherally converted?

A

1/2 androgens are produced in adrenal, half in ovaries.

1/2 are direct testosterone, and 1/2 are converted peripherally.

63
Q

What is Clomiphene?
What is it used for?
What is the mechanism?

A

Clomiphene is a SERM.

It is used as a fertility drug.

It is an Estrogen receptor antagonist in the hypothalamus. It blocks negative feedback of estrogen, leading to increased GnRH pulsatility and increased FSH/LH –> ovulation.

64
Q

What is Tamoxifen?

What is it used for?

A

Tamoxifen is a SERM used to treat hormone-sensitive breast cancers.

65
Q

What is estrogen’s effect on the gonadotrophs during the follicular phase?
E2 effect on follicle?

A

E2 (along with inhibin) suppresses FSH & LH somewhat during follicular phase.

E2 is released by the dominant follicle and causes further follicular development.

66
Q

What causes the change from the Follicular to Ovulatory phase?

A

E2 hits a threshold int the blood where is switches from negative feedback to positive feedback on the Gonadotrophs –> LH surge.

67
Q

What inhibin is active during the follicular phase?

What is its role?

A

Inhibin B is active.

Its role is to partially inhibit gonadotrophs (endocrine) and to stimulate production of androgens from Theca cells (paracrine).

68
Q

What causes the LH surge seen during early Ovulatory phase?

A

E2 switches from negative to positive feedback on the gonadotrophs.

69
Q

What hormone causes ovulation?

A

The LH surge causes ovulation.

70
Q

In the luteal phase, what does the corpus luteum produce?

A

Some E2 and lots of progesterone.

71
Q

What is progesterone’s effect on GnRH/FSH/LH levels?

A

It inhibits GnRH release and thus FSH/LH.

72
Q

When during the menstrual cycle is E2 inhibitory?

A

In the follicular and luteal phases (everything except the ovulatory phase).

73
Q

What can rescue the corpus luteum?

What is this similar to?

A

hCG can rescue the CL

It is similar to LH

74
Q

What causes menstrual bleeding?

A

Without hCG or LH, E2 and progesterone levels fall –> endometrium degrades –> withdrawal bleeding.

75
Q

What E2 levels are needed to cause the LH surge?

A

> 200 pg/mL for 36-48h

76
Q

What does Estradiol (released by dominant follicle) do during the follicular phase to prepare the body?

A

Inhibits cohort follicles from growing
Changes cervical mucus –> sperm transport
Changes Fallopian tube –> ovum transport
Prepares uterine endometrium
Primes GnRH action on LH to allow for LH surge

77
Q

When in a woman’s life does LH release begin?

A

Puberty. LH is only released at night in the beginning.

78
Q

What are FSH/LH like in post-menopausal women?

A

Very high and very pulsatile.

There is little negative feedback by E2.

79
Q

How do men release LH?

Women?

A

Men: Tonic mode = low levels, pulsatile
Women: Surge mode = large periodic release

80
Q

What is the two compartment theory of estrogen production?

A

Theca cells have blood supply, and thus more access to cholesterol. They can also make androgen precursors better.

Granulosa cells have aromatase.

So both are needed for optimal E2 production, and precursors go from Theca to Granulosa cells.

81
Q

What are the phases of the female reproductive TRACT cycle?

A

Proliferative Phase
Secretory Phase
Menstrual (ischemic) phase

82
Q

What is Spinnbarkeit mucus?

A

It is stretchable cervical mucus (low viscosity) seen during ovulation.

83
Q

What causes hot flashes?

A

LH pulses –> ^ vasomotor activity –> reflex sweating, etc.

84
Q

What was found beneficial in HRT with post-menopausal women?

Which group showed the best outcomes?

A

Mixed HRT helped osteoporosis and colorectal cancer.
E2 alone helped breast cancer.

Peri-menopausal women had the best outcomes.

85
Q

What defines primary amenorrhea?

A

No period by age 17.

Caused by:
Turner’s Syndrome
Androgen Resistance
Any HPG axis disorder

86
Q

What defines secondary amenorrhea?

What are the most common causes?

A

Periods cease for > 6 months.

Pregnancy, lactation, menopause

Pathologic: hyper-prolactinemia

87
Q

What defines oligomenorrhea?

A

Infrequent periods (>35 day cycle lengths)

Caused by:
Changes in body fat (exercise, anorexia, etc.)
Stress/illness

88
Q

What causes PCOS?
What are its symptoms?
How is it treated?

A

Polycystic Ovarian Syndrome

High insulin –> Androgen production –> infertility –> no ovulation –> follicles degenerate into cysts

Also, androgens convert into estrogens –> more weight gain (vicious cycle)

Symptoms include sleep apnea, irregular periods, hirsutism.

Treatments: Metformin usually sufficient or Clomiphene; weight loss.

89
Q

At what pregnancy age does the chance of Downs Syndrome surpass 1/100?

A

Age 40

90
Q

What receptor on sperm facilitates the acrosomal reaction?

A

ZP3 Receptor

ZP3 = a glycoprotein in the Zona Pellucida

91
Q

What occurs in the Oocyte following sperm penetration?

A

Increased intracellular Ca2+

This causes the oocyte to release enzymes that cleave ZP2 & modify ZP3 –> prevents polyspermy

Ca2+ also signals the second meiotic division in the oocyte, allowing for pronucleus fusion with the sperm.

92
Q

What are MMP’s?

A

Matrix Metalloproteinases

Secreted by trophoblasts to facilitate invasion of decidua.

93
Q

What does HPL/HCS do?

A

Secreted from syncytiotrophoblasts in response to maternal hypoglycemia. It acts like GH to mobilize fatty acids.

94
Q

What can cause gestational diabetes?

A

HPL/HCS release.

Acts like GH and mobilizes glucose stores in mother. Can tip a pre-diabetic woman into diabetes.

95
Q

What prevents pregnant women from recruiting a new cohort of follicles?

A

hCG has strong negative feedback to the gonadotrophs.

96
Q

What causes Braxton Hicks contractions?

A

Localized positive feedback of fetal cortisol –> placental CRH.

Cortisol potentiates contractions

97
Q

What hormone causes fetal surfactant production?

A

Cortisol.

Can be given to pre-term mothers to facilitate lung development.

FHB (8 decks)

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