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PHYSL214 > Reproductive Physiology > Flashcards

Reproductive Physiology Flashcards

1
Q

What two aspects of reproduction are unique to humans?

A
  1. Humans mate for pleasure as well as procreation.

2. Females are sexually receptive outside of fertile periods.

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2
Q

What is sexual dimorphism?

A

The sexual distinction between males and females.

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3
Q

What are the long-term benefits of reproduction?

A

Biological variation and adaptation to environmental pressures.

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4
Q

What are the gonads?

A

Organs that produce gametes and sex hormones in females and males.

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5
Q

What is the internal genitalia?

A

Accessory glands and ducts that connect glands with the outside environment.

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6
Q

What is the external genitalia?

A

All external reproductive structures (penis and vulva)

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7
Q

Describe the dual function of the gonads.

A

The gonads participate in gametogenesis as well as the secretion and production of sex hormones/gonadal steroids.

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8
Q

What sex hormones are present in both males and females?

A

Testosterone, estradiol, and progesterone.

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9
Q

How does male gametogenesis differ from female gametogenesis?

A

Males are born with primary spermatocytes that continue to be generated through mitotic divisions until death.

Germ cell mitosis occurs in fetal development in females and stops at birth; finite pool of primary oocytes.

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10
Q

Describe the gametogenesis of the female reproduction system.

A

Oogonium divides into multiple oogonia, creating a pool of diploid cells.

In the developmental stage, meiosis begins to create a pool of 4N primary oocytes. No cell division happens until the onset of puberty, when a primary oocyte begins the first meiotic division.

A first polar body is discarded and a secondary oocyte (2N) is created and released from ovary at ovulation; if fertilized, second meiotic division occurs and second polar body is produced. Haploid fusion of sperm and egg cell occurs, zygote is created.

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11
Q

What is the term for the female germ cell?

A

Oogonium.

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12
Q

What is the term for the cells generated in mitotic division of oogonium?

A

Oogonia.

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13
Q

Describe the gametogenesis of the male reproductive system.

A

The spermatogonium begins to divide mitotically from early embryonic development. Division continues into puberty where the first meiosis occurs to produce primary spermatocytes (4N).

Primary spermatocyte divides to create secondary spermatocyte, then again to create spermatids that will mature into haploid sperm.

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14
Q

What does one primary oocyte yield?

A

One egg.

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15
Q

What does one primary spermatocyte yield?

A

4 sperm.

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16
Q

What is the term for the male germ cell?

A

Spermatogonium.

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17
Q

What is the term for the cells produced through spermatogonium mitotic division?

A

spermatogonia.

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18
Q

What happens to the second (if present) X chromosome?

A

Condenses into inactive sex chromatin (Barr body) that does not participate in gene transcription.

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19
Q

When does sex differentiation occur?

A

During embryonic and fetal development.

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20
Q

When do gonads begin to differentiate?

A

6th week of uterine life.

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21
Q

What is the bipotential stage?

A

The sexually indifferent stage in which both the Wolffian and Mullerian duct systems are present and viable.

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22
Q

What is activated during the seventh-eighth week of uterine life? What does this cause (in males)

A

SRY Gene encodes TDF (SRY protein) that triggers the development of testes and the differentiation of Leydig and Sertoli cells.

The Wolffian system persists and testes begin to secrete MIS that degenerates the Mullerian system.

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23
Q

What hormone differentiates the Wolffian system into gonads and internal genitalia?

A

Testosterone.

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24
Q

What is MIS? What is it secreted by?

A

Mullerian-inhibiting substance, secreted by fetal testes after SRY triggers MIS gene.

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25
Q

What do male and female gonads both derive from?

A

The urogenital bridge.

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26
Q

What does the Wolffian duct system develop into?

A

Epididymis, vas deferens, seminal vesicle, ejaculatory duct.

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27
Q

What does the formation of external male genitalia depend on?

A

The formation of a functional testis.

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28
Q

What are the two key cells present in male gonads?

A

Sertoli and Leydig cells.

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29
Q

What do Leydig cells secrete?

A

Testosterone.

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30
Q

What do Sertoli cells secrete?

A

MIS.

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31
Q

If functional testis are present, how is the external genitalia formed?

A

Testosterone is converted into potent DHT, which forms the penis and scrotum and disappearance of urogenital slit.

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32
Q

What happens if DHT cannot be generated in a genetic male?

A

Intersex phenotype.

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33
Q

How do the testes descend?

A

Their descent is stimulated by testosterone secreted from leydig cells.

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34
Q

What occurs is the testes do not descend?

A

Cryptorchidism; possible infertility due to decreased sperm production.

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35
Q

What occurs in the absence of fetal testes and SRY gene?

A

No testosterone or MIS secretion by Leydig and Sertoli; Mullerian system persists and results in the degeneration of the Wolffian system. Forms fallopian tubes and uterus.

Urogential slit remains open, developing external genitalia.

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36
Q

What does the Mullerian system develop into?

A

Fallopian tubes, uterus, upper part of vagina.

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37
Q

Do fetal ovaries influence the sex differentiation process?

A

No, there is no hormone secretion by fetal ovaries.

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38
Q

What happens if there is an androgen exposure to genetic females before external genitalia development? After?

A

Intersex.

After: Viralization.

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39
Q

What is androgen insensitivity syndrome?

A

Androgens are produced by leydig cells but there is a receptor malfunction that impairs the binding of testosterone; Wollfian ducts generate, but Mullerian also degenerates due to presence of MIS. Intersex or lacking sex, essentially.

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40
Q

What is congenital adrenal hyperplasia?

A

Overproduction of androgen in XX fetus due to malfunction in cortisol production pathway, resulting in lack of negative feedback loop on ACTH secretion. Results in high circulating levels of androgens and intersex development.

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41
Q

How is congenital adrenal hyperplasia treated?

A

Cortisol replacement therapy, phenotype fixed through surgery.

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42
Q

What is the starting precursor for all gonadal steroid hormones?

A

Cholesterol.

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43
Q

What enzyme converts Testosterone and other androgens into estrogen?

A

Aromatase.

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44
Q

What enzyme converts testosterone into DHT?

A

5-alpha-reductase.

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45
Q

Where is testosterone synthesized?

A

Mostly in the testes, less potently in the adrenal cortex.

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46
Q

What form of estrogen in predominant in fertile women?

A

Estradiol.

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47
Q

What form of estrogen is predominant in post-menopausal women?

A

Estrone.

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48
Q

What form of estrogen is predominant in pregnant women?

A

Estriol; is produced by the placenta.

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49
Q

Where is estrogen released from in males?

A

Small amounts from the testes and converted from androgens in non-gonadal tissues.

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50
Q

What is the major secretory product of the placenta during pregnancy?

A

Progesterone.

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51
Q

What is the function of the HPG axis?

A

The hypothalamus-pituitary-gonadal axis is a series of endocrine organs connected through feedback loops; controls reproduction through key hormones GnRH, LH, and FSH.

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52
Q

What is GnRH?

A

Gonadotropin-releasing hormone: secreted by neuroendocrine cells in the hypothalamus, controls anterior pituitary function.

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53
Q

What is FSH?

A

Follicle-stimulating hormone, is released from the anterior pituitary upon stimulation of GnRH.

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54
Q

What is LH?

A

Luteinizing hormone: released from anterior pituitary upon stimulation of GnRH.

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55
Q

What effect does testosterone have on the hypothalamus?

A

Negative: feedback inhibition.

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56
Q

What effect does estrogen have on the anterior pituitary?

A

Negative in low amounts, positive feedback in sustained high amounts.

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57
Q

What hormone has dual role in females only?

A

Luteinizing hormone, facilitates gamete production as well as steroid hormone production.

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58
Q

Describe the pulsatile release of GnRH.

A

GnRH is released from the hypothalamus every 1-3 hours, stimulating a release of LH and FSH.

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59
Q

Why is GnRH released in pulses?

A

To avoid tolerance and downregulation of GnRH receptors on gonadotropin cells. If this were to occur, the pituitary would not respond to GnRH.

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60
Q

How are GnRH pulses formed?

A

By a region in the hypothalamus containing GnRH neuron cells called ‘GnRH pulse generators’.

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61
Q

What peptide controls GnRH pulsatile releases?

A

Kisspeptin

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62
Q

How is reproductive function affected in females?

A

Stress
Nutrition
Day-light cycles
Environmental estrogens

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63
Q

What comprises the male accessory reproductive organs?

A

Ducts for sperm storage and transport as well as accessory glands:
Prostate, bulbourethral gland, seminal vesicles.

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64
Q

What comprises the external male genitalia?

A

Penis and scrotum.

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65
Q

What is the urethra (male)?

A

Common passage for urine and seme, ventral aspect of the penile shaft.

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66
Q

What is the urthra surrounded by?

A

Corpus spongiosum.

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67
Q

What comprises the penile erectile tissue?

A

Corpus spongiosum and corpora cavernosa .

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68
Q

What is the glans?

A

The enlarged tip of the penis, covered in foreskin at birth.

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69
Q

What is the scrotum?

A

Extension of the abdominal wall that holds the testes.

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70
Q

Can testosterone production and secretion occur at internal body temperature?

A

Yes.

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71
Q

Can sperm production occur at internal body temperature?

A

No, must be two degrees lower.

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72
Q

What is the spermatic cord?

A

Branch of vessels and nerves that extend into epididymis and testes, include the vas deferens.

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73
Q

How does spermatogenesis occur if lower tempertaure is required?

A

Extensive vascularization between artery and plexus lead to loss of heat before vascularization of testes.

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74
Q

What is the site of spermatogenesis?

A

Seminiferous tubules.

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75
Q

Describe flow of sperm from seminiferous tubules to vas deferens:

A 
Seminiferous tubules
Rete Testis
Efferent Ductules
Epididymis
Vas Deferens
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76
Q

What encapsulates the seminiferous tubules?

A

Outer fibrous capsule.

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77
Q

What is present in the interstitial tissue of seminiferous tubules?

A

Leydig cells and blood vessels.

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78
Q

Where do the vas deferens extend after leaving the epididymis?

A

Extend behind the bladder to join with the seminal vesicles to form the ajaculatory gland.

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79
Q

Where does the ejaculatory duct connect to?

A

A seminal vesicle, prostate gland, vas deferens.

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80
Q

Why is the prostate “gland” so unique from other glands?

A

There is no gland morphology; fluids are secreted from the walls of the organ.

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81
Q

What is the bulbourethral gland?

A

Gland that drains fluid into urethra at its junction with the prostate.

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82
Q

What are the functions of accessory gland secretions?

A

Nourish sperm with nutrients, protect with buffers to defend against acidic vaginal pH and urethral acidity.

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83
Q

What is the function of seminal-vesicle secretions?

A

Promote increased sperm motility, prostoglandins (immunity and motility)

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84
Q

What is the function of prostoglandins? Where are they secreted from?

A

Motility and immune defense by inducing contractions; secreted from seminal vesicle.

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85
Q

What is the function of the secretions from the bulbourethral gland?

A

Lubrication.

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86
Q

What is the final phase of spermatogenesis?

A

Differentiation of spermatids into spermatozoa.

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87
Q

What is each seminiferous tubule surrounded by? What two cell-types does it contain?

A

Basement membrane.

Developing sperm and sertoli cells.

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88
Q

What is the function of the Leydig cells?

A

Synthesize and release testosterone.

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89
Q

What are the secondary functions of the sertoli cells?

A

Nourish developoing spermatagonia, secrete inhibin, grwoth factors, enzymes, and androgen-binding protein?

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90
Q

What is the function of androgen-binding protein?

A

Binds testosterone to sertoli cells to prevent it from diffusing out of the cell.

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91
Q

How are sertoli cells joined together? How does this affect spermatogonia transport?

A

Tight junctions; developing sperm move through these junctions.

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92
Q

Where are Leydig cells located?

A

Connective tissues in spaces between tubules.

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93
Q

Describe the timeline of activity in Leydig cells.

A

Active in fetus, synthesizing and releasing testosterone.

Quiescent following birth, then reactivated during puberty.

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94
Q

Why is the relationship between Leydig cells and Sertoli cells so important?

A

Sertoli cells require testosterone to increase spermatogenesis, but cannot create testosterone. However, Leydig cells are able to give Sertoli cells their testosterone to promote spermatogenesis.

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95
Q

What action do Sertoli cells take in response to FSH and local testosterone?

A

Inhibin that feedback negatively to FSH, and modulate Leydig function.

96
Q

What cell phagocytizes defective sperm?

A

Sertoli cells.

97
Q

What occurs to spermatids during final stages of maturation?

A

Cytoplasm is lost and tail is developed.

98
Q

What is the morphology of the sperm head?

A

Almost entirely nucleus

Acrosome covers tip of the nucleus; contains enzymes and proteins important for fertilization.

99
Q

What is the morphology of the sperm midpiece?

A

Formed by the mitochondria for energy of movement.

100
Q

What is the morphology of the sperm tail?

A

Flagellum.

101
Q

Where is sperm stored until ejaculation?

A

Vas deferens and epididymis.

102
Q

How does continued production of sperm in the seminiferous tubules not cause inflation of the epididymis?

A

Fluid is constantly absorbed from the epididymis lumen, concentrating sperm and lowering fluid pressure.

103
Q

How is sperm propelled during ejaculation?

A

The peristaltic movement of the vas deferens and epididymis.

104
Q

What is a vasectomy?

A

Removal of a segment of each vas deferens, prevents sperm from travelling up deferens during ejacultaion.

105
Q

What factors affect sperm?

A 
Heat and pressure
Caffeine, nicotine, drugs,
Environmental toxins
Saliva
Estrogens
106
Q

Describe the mechanism of penile erection:

A

Sexual excitation leads to the dilation of small arteries, increasing blood flow to the penis, and engorgement of vascular compartments. This passively compresses adjacent veins to trap blood in the penis.

107
Q

What are the primary molecules responsible for the relaxation of penile vascularization and thus erection?

A

Prostaglandins and Nitric oxide.

108
Q

How does CNS input alter/control erection?

A

Stimulation from penile mechanoreceptors and erotic sensory stimuli trigger descending CNS pathways that increases activity of neurons releasing nitric oxide; NO inhibits the sympathetic action of arteries in the penis.

Arteries dilate as a result, causing erection and compression of veins.

109
Q

What kind of neurons release nitric oxide?

A

Non-adrenergic, non-cholinergic autonomic neurons.

110
Q

What are the two phases of ejaculation?

A
  1. Emission

2. Ejaculation

111
Q

Describe the process of the emission phase.

A

Sympathetically mediated reflex; contraction of the epididymis, vas deferens, ejaculatory ducts, prostate and seminal vessels; sperm and secretions emptied into urethra.

112
Q

Describe the ejaculation phase.

A

Semen is expelled from urethra by rapid contractions of urethral smooth muscle and skeletal muscles. Sphincter at the base of the bladder closes.

113
Q

What is an orgasm?

A

Period of muscle contractions accompanies by pleasure and systemic physiological changes. Is always followed by a latency period in which erection in not possible.

114
Q

What is erectile dysfunction?

A

Consistent inability to achieve or maintain an erection during intercourse.

115
Q

What is ED caused by?

A

Damage to nerves, endocrine disorders, drugs, diseases, and psychological factors.

116
Q

What are treatment option for ED?

A

Drugs that inhibit the breakdown of cGMP (activated by NO): Viagra.
Drugs that act on PGE1 receptors to activate cAMP (Alprostadil)

117
Q

What were PDE5 inhibitors initially designed for?

A

Pulmonary hypertension.

118
Q

What hormone feeds back to inhibit FSH release? (M)

A

Inhibin.

119
Q

What hormone feeds back to inhibit LH release? (M)

A

Testosterone.

120
Q

What function does testosterone have on brain, liver, and adipose tissue?

A

Converted to estradiol by aromatase.

121
Q

What function does testosterone have on the prostate gland?

A

Converted to DHT by 5-alpha-reductase.

122
Q

What hormones mediate libido?

A

Androgens.

123
Q

What is the general secondary function of testosterone? (Not spermatogenesis)

A

Muscle mass increase
Skeletal growth
Sexual function increase

124
Q

What is the main secondary function of DHT (not external genitalia dev)

A

Facial and body hair growth
Acne
Scalp hair loss
Prostate growth

125
Q

What is the primary function of estradiol in non-gonadal tissue?

A

Breast tissue growth

Bone formation

126
Q

What is the effect if testosterone is lost? What are potential causes for this disorder?

A
  • Impaired sexual libido/function
  • Decrease in size of accessory organs
  • Reduction in secretion rate by glands.

Possibly caused by castration.

127
Q

When does puberty typically occur in males?

A

12-16 years

128
Q

What are the early stages of puberty caused by?

A

Secretion of adrenal androgens (from adrenal cortex)

129
Q

What is the proposed mechanism for puberty?

A

Sudden reduction in sensitivity to negative GnRH feedback by gonadal hormones; Kisspeptin neurons in hypothalamus increase activity and cause surge of GnRH, increasing concentrations of FSH and LH.

130
Q

What are secondary sex characteristics for men? What are these dependent on?

A

Growth of larynx, thick secretion of skin oil glands, enlargement of the genitalia, facial, body, and armpit hair. Masculine fat distribution.

Dependent on Testosterone and DHT.

131
Q

What causes an increased hematocrit in males?

A

Androgen-stimulated erythropoietin secretion from kidneys.

132
Q

What is the consequence of anabolic steroid use?

A

Overstimulation of prostate, decreased GnRH LH FSH due to feedback inhibition (exogenous steroids cannot cross blood sertoli barriers)

Decreased endogenous testosterone.

133
Q

What is hypogonadism?

A

Decrease in testosterone release from testes.

134
Q

What is primary hypogonadism?

A

Testicular failure; insufficient production of tetsosterone.

135
Q

What is secondary hypogonadism?

A

Failure to supply testes in gonadotropin stimulus (hypothalamus or pituitary defect)

136
Q

What is Klinefelter’s Syndrome?

A

XXY, poorly developed testes due to primary hypogonadism; insufficnet leydig and sertoli cell function.

Absence of secondary sex characteristics, high FSH and LH concentrations.

137
Q

What is hyperprolactinemia?

A

form of secondary hypogonadism due to high concentrations of prolactin (pituitary gland dysfunction); inhibits LH and FSH.

138
Q

What is hypopituitarism?

A

Form of secondary hypogonadism; loss of anterior gland function and no release of LH/FSH.

139
Q

What is Andropause?

A

Decrease in testosterone levels starting at age 40, deterioration of testicular function caused by failure of gonads to respond to gonadotropins. Decreased libido and sperm count (primary hypogonadism).

140
Q

What comprises the female external genitalia?

A 
Mons pubis
Labia minora
Labia majora (scrotum)
Clitoris (penis)
Vaginal vestibule
Vestibular glands

(VULVA)

141
Q

What is the hymen?

A

The thin fold of mucous membrane that partly overlies the vaginal opening.

142
Q

What is the function of the ovaries before ovulation?

A

Maturation of oocytes and endocrine function.

143
Q

What is the function of ovaries after ovulation?

A

Develop corpus luteum.

144
Q

What cells begin to form around primordial follicles? What is the function of these cells?

A

Granulosa cells; secrete estrogen, progesterone, and inhibin.

145
Q

What begins to form at the primordial follicle proliferates into primary and preantral follicle?

A

Zona pellucida and early theca.

146
Q

What is the function of the zona pellucida?

A

Separated the ovum from inner layer of granulosa cells. Contain glycoproteins that bind the sperm to the egg during fertilization.

147
Q

What is the antrum?

A

Fluid filled pocket in the follicle formed during early antral follicular stage; guides ovum onto ovarian surface during ovulation.

148
Q

What is the cumulus oophorus? Function?

A

Layer of granulosa cells that anchor the ovum to the theca layer.

149
Q

Where does the fluid in the antrum come from?

A

Secretions from granulosa cells

150
Q

What is the function of the granulosa cells?

A

To nourish the egg, create estrogen from androgens.

151
Q

What is the function of the theca cells?

A

Respond to LH; create androgens to be delivered to inner granulosa cells.

152
Q

When do follicles begin to develop?

A

At the beginning of the menstrual cycle; cohort of follicles are nourished to develop into larger antral follicles.

153
Q

What is the follicle selection process? When does this occur?

A

The largest antral follicle is sleected to be the dominant follicle (largest output of estrogen and therefore most sensitive to FSH and estrogen) this is how it is detected.

Happens 1 week into menstrual cycle; non-dominant follicles undergo atresia.

154
Q

When does the first meiotic division of the oocyte occur?

A

During ovulation (midpoint of menstrual cycle); enzymes degrade theca and granulosa wall and ovarian wall causing rupture. Creates secondary oocyte.

155
Q

What is the fully mature follicle called?

A

Graafian follicle.

156
Q

What occurs to the remaining structure of the follicle after ovulation?

A

Granulosa cells enlarge and reform the ovarian wall, become endocrine gland-like corpus luteum.

157
Q

What is the function of the corpus luteum?

A

Secretes estrogen, progesterone, inhibin.

If egg is not fertilized, rapidly degenerates into atretic follicle and corpus albicans.

158
Q

What does loss of corpus luteum function cause?

A

Menstruation and beginning of new follicular development.

159
Q

What are the two phases of the menstrual cycle?

A
  1. Follicular phase.

2. Luteal phase.

160
Q

Describe the follicular phase.

A

The mature follicle and secondary oocyte develop, secretions come from hypothalamus, pituitary, and granulosa cells.

161
Q

Describe the luteal phase.

A

Ovulation has occurred and follicle degenerates into corpus luteum. For ten days if egg is not fertilized, rapid spike in progesterone and estrogen and inhibin.

162
Q

What causes the rapid LH surge seen in ovulation?

A

Consistent increase in estrogen levels secreted by granulosa cells, overrides negative feedback inhibition to positively activate pituiatry gland.

163
Q

What is the secondary estrogen rise caused by?

A

Secretions due to the corpus luteum.

164
Q

What causes the small release of progesterone in the follicular phase?

A

Ovarian secretions.

165
Q

What casues the large release of progesterone following ovulation?

A

The secretion by the corpus luteum.

166
Q

What causes a rapid drop in LH/FSH levels?

A

After ovulation, estrogen levels drog due to inactivity of granulosa cells; feedback switches to inhibition and corpus luteum secreted inhibin to further inhibit LH/FSH release.

167
Q

Why does FSH decrease 1 week into the menstrual phase?

A

The primary oocyte is selected; all other follicles can be degraded, FSH is no longer needed because the follicle has developed LH receptors and is more sensitive to low levels of FSH/LH.

168
Q

What cells are Granulosa cells similar to?

A

Sertoli cells; modulate germ cell microenvironment (stimulated by FSH and gonadal sex hormone).

169
Q

What cells are theca cells similar to?

A

Leydig cells: produce androgens (stimulated by LH)

170
Q

How do theca cells aid granulosa cells?

A

Produce androgens.

171
Q

What effect does the LH surge have on granulosa cells?

A

Initiates a production of progesterone, which begins to block the effects and synthesis of estrogen (this is why estrogen dips slightly and progesterone increases slightly around mid-cycle)

172
Q

What hormone causes the transformation of granulosa cels and theca cells into corpus luteum?

A

LH.

173
Q

Why does the corpus luteum inhibit secretion of FSH and LH surges?

A

There is no need for follicular development or ovulation when an egg is released into the fallopian tube.

174
Q

What is the proliferative phase?

A

End of menstruation; endometrium begins to thicken in response to increased estrogen. Occurs between cessation of menstruation and ovulation.

175
Q

What is the menstrual phase?

A

Degeneration of endometrium due to loss of corpus luteum.

176
Q

What is the secretory phase?

A

Occurs post-ovulation, endometrium secretes glycogen in glandular epithelium in response to estrogen and progesterone, increased vascularization and nutrition to create habitable environment for fetus.

177
Q

What is the role of progesterone in the menstrual cycle?

A
  1. Inhibit myometrial contractions to prevent premature birth.
  2. Opposes stimulatory actions of estrogen and local prostaglandins to prevent inflammation.
  3. Ensures safe implantation.
    IE) UTERINE QUIESCENCE.
178
Q

What effect does estrogen have on the cervix?

A

Secretes abundant watery/clear mucous that aids in motility of sperm.

179
Q

What effect does progesterone have on the cervix?

A

Occurs after ovulation; secretes a thick and sticky mucous that prevents sperm motility.

180
Q

What four events occur during menstruation?

A
  1. Constriction of uterine blood vessels (deprived of oxygen and nutrients, cell death) mediated by prostoglandins. Causes cramps.
  2. Disintegration of uterine lining.
  3. Rhythmix contractions of uterine smooth muscle due to prostoglandin overproduction.
  4. Dilation of endometrial arteries (hemorrhage through capillary walls)
181
Q

When does puberty occur in females?

A

10-12 years old.

182
Q

What is believed to stimulate GnRH production in females?

A

Leptin hormone secreted by adipose tissue.

183
Q

What stage of follicular development does the ovary reach prior to puberty?

A

Early antral stage, then degeneration of follicle.

184
Q

What is amenorrhea?

A

Lack of menstrual flow.

185
Q

What is primary amenorrhea?

A

Failure to begin normal menstrual cycle at puberty.

186
Q

What is secondary amenorrhea?

A

Loss of previously normal menstrual cycles.

187
Q

When is the optimal time period for fertilization?

A

Between 5 days before ovulation and 1 day following ovulation.

188
Q

Once ejaculated how long are sperm viable for?

A

4-6 days.

189
Q

Once ovulated, how long is the egg viable for?

A

24-48 Hours.

190
Q

What is capacitation?

A

Seminal plasma coating of the sperm is removed, exposing portions of the sperm that can bind to the zona pellucida of the oocyte. Movement of sperm also shifts from wave-like to whip-like.

191
Q

When does capacitation occur?

A

Once the sperm has been exposed to the female tract for several hours.

192
Q

How do the sperm reach the zona pellucida?

A

They move through the granulosa cells of the corona radiata layer.

193
Q

What is the acrosome reaction? How is it triggered?

A

Plasma membrane of sperm head altered; underlying enzymes exposed to zonda pellucida and create path for sperm to advance toward the egg’s plasma.

It is triggered whem the sperm binds to the zona pellucida.

194
Q

What happens when multiple sperm penetrate the egg?

A

The zygote is no longer viable.

195
Q

How is polyspermy prevented?

A

Fusion of sperm with egg plasma causes change in membrane potential; triggers the cortical reaction.

196
Q

What is the cortical reaction?

A

Cytosolic secretory vesicles around the egg release enzymes between egg plasma and zona pellucida, inactivate sperm binding site and harden the zona pellucida to prevent entrance.

197
Q

How long is the conceptus housed in the fallopian tube? Why is it held here?

A

3-4 days, rich with nutrients to aid mitotic division of the zygote into a morula.

198
Q

How is the conceptus pushed into the uterus from the fallopian tube?

A

Estrogen contracts smooth muscle at junction of fallopian tube and uterus, progesterone causes relax of the function, permitting conceptus passage.

199
Q

After the cell floats in intrauterine fluid for 3 days, what occurs? What stage is the conceptus at?

A

Blastocyst stage: no more divisions, only differentiation.

200
Q

What is the outer layer of the blastocyst?

A

Trophoblast: contribute to nutrition and hormone secretion.

201
Q

What is the inner cell mass of the blastocyst?

A

Mass of cells that give rise to developing human.

202
Q

When does implantation begin? How does it occur?

A

Day 21 of menstrual cycle; blastocyst embeds into the endometrium due to trophoblasts sticky consistency.

203
Q

What provides the zygote with nutrients for the first few weeks of implantation?

A

The nutrient-rich endometrial cells.

204
Q

What is the placenta formed by?

A

Interlocking fetal and maternal tissues.

205
Q

What is the function of the placenta?

A

To mediate the exchange of nutrients between mother and fetus for the entire pregnancy.

206
Q

What is the embryonic portion of the placenta?

A

The chorion (outer trophoblast cells)

207
Q

What is the maternal portion of the placenta?

A

Th endometrium underlying the chorion.

208
Q

What are the chorionic villi?

A

Project from the chorion into the endometrium, contains rich capillary network that is part of the embryo’s circulation; secrete enzymes and paracrine factors into the endometrium.

209
Q

What are each chorionic villi surrounded by?

A

A pool of maternal blood (sinus)

210
Q

What is the amniotic cavity?

A

Cavity formed between inner cell mass and chorion, contains the amniotic sac and amniotic fluid.

211
Q

What is the function of amniotic fluid?

A

To buffer mechanical disruption and regulate temperature fluctuations.

212
Q

How is the fetus attached to the placenta?

A

The umbilical cord.

213
Q

How do hormones change throughout pregnancy?

A

Plasma estrogen and progesterone continually increase throughout pregnancy. Sudden drop at delivery. Human chorionic gonadotropin increases rapidly in the first two months then decreases to low amounts for remainder of pregnancy.

214
Q

What is the function of estrogen during pregnancy?

A

Stimulate the growth of uterine muscle mass. Supply contractile force during delivery.

215
Q

What is the function of progesterone during pregnancy?

A

Inhibits uterine contracility to prevent premature delivery.

216
Q

What cells secrete hCG? When does this occur?

A

Trophoblast cells during endometrial invasion.

217
Q

What secretes sex hormones following the degeneration of the corpus luteum after surgery?

A

The placenta, can synthesize progesterone but no others.

218
Q

What provides the placenta with androgens for secretion?

A

Maternal ovaries
Adrenal glands
Fetal adrenal glands

219
Q

What is parturition? When does it occur?

A

The final weeks of pregnancy:

  • Softening of cervix
  • Myometrial expression of oxytocin receptors
  • Increased estrogen
  • coordinated contraction of uterine muscle (Braxton-Hicks)
220
Q

What happens during the final month of pregnancy?

A

Fetus drops down to contact the cervix in preparation or delivery.

221
Q

What are the steps of labor and delivery?

A
  1. Amniotic sac ruptures
  2. Amniotic fluid flows out of vagina
  3. Powerful uterine contractions ensue.
  4. Cervix is forced open and progressively dilates.
  5. Contractions move fetus through cervix and vagina
  6. Fetus delivered and constriction of umbilical and placental vessles.
  7. PLacental delivery.
222
Q

What are the 4 controllers of parturition?

A
  1. The properties of the myometrium: smooth muscle cells auto-rhythmic in response to fetal stretch.
  2. Uterine prostoglandin secretion: stimulates smooth muscle contraction.
  3. Oxytocin: feedback loop.
  4. Progesterone inhibits uterine contractions during pregnancy but becomes overwhelmed by estrogen during delivery.
223
Q

What is the positive feedback mechanism present at parturition?

A
  1. Baby drops lover in uterus to initiate labour.
  2. Cervix is stretched.
  3. Hypothalamic input stimulates oxytocin release.
  4. Oxytocin causes uterine contractions.
  5. Uterine contractions push baby against cervix.
  6. Pressure against cervix causes cervical stretch.
224
Q

How is the parturition feedback loop stopped?

A

When the baby is delivered.

225
Q

What is lactogenesis?

A

Lactation: production and secretion of milk by mammary glands.

226
Q

Where is the site of milk secretion?

A

Breast alveoli (epithelial cells on inner lining)

227
Q

What cells are responsible for milk expulsion?

A

Contractile myoepithelial cells.

228
Q

What is prolactin?

A

Hormone stimulating milk production; secreted in high amounts during pregnancy.

229
Q

Why does a mother not lactate during pregnancy?

A

Estrogen and progesterone inhibits the acion of prolactin on breasts.

230
Q

Describe the mechanism of breastfeeding.

A

Suckling stimulates nipple mechanoreceptors, which sends neural input to hypothalamus.

Hypothalamus decreases dopamine secretion and increases prolactin releasing factor.

Posterior pituitary increases oxytocin secretion, which causes contraction of myoepithelial cells and milk ejection.

Anterior pituitary releases prolactin which stimulates mammary gland to synthesize milk.

231
Q

What is colostrum?

A

The first breast milk fluid released from mother after birth, contains many nutrients and antibodies to build baby’s immunity. Also contains growth factors and endogenous opioids.

232
Q

How do oral contraceptives function?

A

Estrogen and progesterone inhibit gonadotropin release to prevent ovulation.

Thicken cervical mucus and inhibit proliferation of the endometrium.

233
Q

What is the function of Mifepristone?

A

Emergency contraceptive or abortifacient: antiprogesterone activity that binds to progesterone receptors in the uterus and erodes endometrium, increases contractions.

234
Q

When does menopause occur?

A

Around 50 years.

235
Q

How does menopause occur?

A

Menstrual cycle ceases for 12 months, ovarians no longer respond to gonadotropins and most follicles are lost to atresia.

Loss of estrogen and inhibin releases negative feedback control of the hypothalamus (Increases concentrations of GnRH and FSH and LH in plasma)

236
Q

What are the secondary effects of menopause?

A

Atrophy of breasts and reproductive organs
Osteoporosis
Hot flashes
Increased risk of cardiovascular disease

PHYSL214 (5 decks)

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