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PHYSL 214 > Reproduction > Flashcards

Reproduction Flashcards

1
Q

what 2 factors set human reproduction apart from animals?

A

mate for pleasure & procreation, females are sexually receptive outside fertile window

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2
Q

what 3 factors of human reproduction are similar to animals?

A

internal fertilization, mating/courtship rituals, internal fetal development

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3
Q

what is the benefit of internal fertilization?

A

motile, flagellated sperm remain in an aq enviro

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4
Q

what are 2 benefits of internal fetal development?

A

protects embryo from dehydration, cushioned from mech damage

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5
Q

what is sexual dimorphism?

A

physical/sexual distinction btwn males and females

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6
Q

what is reproduction?

A

perpetuation of a species via production offspring (important for species but not individual survival)

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7
Q

what determines the sex differentiation of the embryo?

A

sex hormones

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8
Q

what do the gonads produce?

A

sperm/ovum (gametes) and sex hormones

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9
Q

how many weeks after the production of a zygote is it considered an embryo then fetus?

A

embryo: 0-8 weeks
fetus: 8-birth

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10
Q

what are the 3 “structures” of male/female sex organs?

A

gonads (testes/ovaries), internal genitalia (connect gonads to ext enviro), external genitalia

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11
Q

what are 3 sex/steroid hormones? and ex?

A

androgens (testosterone, DHT), estrogen (estradiol), progesterone

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12
Q

t/f: androgens are only present in males, and estrogen/progesterone are only found in females

A

false, all are found in both males and females

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13
Q

what are developing gametes aka?

A

germ cells

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14
Q

how many chr do gametes contain?

A

23 (not in pairs, one set)

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15
Q

when do females vs males undergo germ cell mitosis? (primary oocyte/spermatocyte)

A

females: fetal development
males: embryonic stage
(both in utero)

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16
Q

what is a diff btwn female vs male germ cell mitosis?

A

female: mitosis completed before birth
males: significantly begins at puberty and continues throughout life

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17
Q

what is the process of female gametogenesis (include 1N, 2N, 4N)? (4)

A

oogonium/germ cell (2N) undergoes mitosis and begins meiosis w/ DNA repl’n to generate primary oocyte (4N) as embryo, meiosis 1 occurs at puberty generating 1st polar body and secondary oocyte (egg, 2N), egg released at ovulation, if fertilized: undergoes meiosis 2 (1N) and generates 2nd polar body and zygote (2N), unfertilized: degenerates

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18
Q

t/f: one primary oocyte yields 2 eggs

A

false, meiosis 1 of primary oocyte generates only 1 egg (polar body disintegrates)

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19
Q

what is the process of male gametogenesis (include 1N, 2N, 4N)? (4)

A

spermatogonium/germ cell (2N) begins mitosis as embryo, meiosis begins w/ DNA repl’n at puberty (mitosis continues) to generate primary spermatocyte (4N), meiosis 1 generates secondary spermatocytes (2N), meiosis 2 generates spermatids (1N) which develop into sperm

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20
Q

t/f: one primary spermatocyte generates 2 sperm

A

false, one primary spermatocyte generates 4 sperm (meiosis 1 and 2)

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21
Q

how many chr is 1N, 2N, and 4N?

A

1N: 23 chr (no pairs/homologs)
2N: 46 chr (23 pairs/homologs)
4N: 46 (sister chromatids)

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22
Q

what is sex chromatin/Barr body?

A

one X of XX is non-functional, condenses to form sex chromatin (aka Barr body)

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23
Q

where is sex chromatin/Barr body contained? (2)

A

cheek mucosa cells and WBCs

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24
Q

how can genetic sex abnormalities be found?

A

by karyotyping (tissue culture)

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25
Q

what do XXX, XXY, YO, and XO genotypes all result in?

A

XXX: female
XXY: male
YO: non-viable (need X)
XO: female, Turner’s syndrome

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26
Q

what scenario can cause sexual phenotype to not match chr composition?

A

atypical sex differentiation (≠ XX/XY)

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27
Q

what can atypical sex differentiation result in?

A

intersex or ambiguous genitalia

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28
Q

what is required for proper sex differentiation? (2)

A

genes on chr, secretions from gonads (testes primarily)

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29
Q

what week do gonads remain undifferentiated until?

A

6th week

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30
Q

what week do testes develop?

A

week 7

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31
Q

what gene on the Y chr mediates development of testes?

A

SRY (Sex-determining Region Y) gene

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32
Q

which cells express SRY gene?

A

urogenital ridge cells

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33
Q

what protein does SRY gene encode for?

A

TDF (testes determining factor)

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34
Q

what do both male and female gonads derive from?

A

urogenital ridge

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35
Q

what cells does TDF trigger development of?

A

Leydig and Sertoli cells (in testes)

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36
Q

what occurs if Y chr/SRY gene is absent?

A

testes don’t develop, and ovaries do in same region

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37
Q

what does the undifferentiated fetal reproductive tract contain? (3)

A

wolffian ducts, mullerian ducts, common opening for ducts/urine

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38
Q

what duct system persists in males?

A

wollfian

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39
Q

t/f: duct systems can give rise to external genital structures

A

false, only give rise to internal structures

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40
Q

what does ultimate development of male internal and external structures depend on?

A

presence of functional, fetal testes

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41
Q

what do Leydig vs Sertoli cells secrete?

A

Leydig: testosterone
Sertoli: mullerian-inhibitng substance/H (MIS)

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42
Q

what induces MIS gene?

A

SRY protein

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43
Q

what does MIS do?

A

degenerates mullerian duct system

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44
Q

what does testosterone do for fetal development?

A

differentiates wolffian ducts into epididymis, vas deferens, ejaculatory ducts and seminal vesicles

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45
Q

what hormone forms penis and scrotum, and degenerates urogenital slit?

A

testosterone-derived DHT

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46
Q

what does absence of DHT cause?

A

intersex (required for external genitalia)

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47
Q

what hormone stimulates testes to descend?

A

testosterone

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48
Q

what is failure to descend testes called?

A

cryptochordism (remain in abdomen)

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49
Q

what can cryptochordism result in?

A

decr sperm production

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50
Q

why does cryptochordism cause decr sperm production?

A

proper sperm development requires lower than core body temp, if testes remain in abdomen, too hot for proper development

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51
Q

what triggers degeneration of wollfian ducts?

A

absence of testes, SRY gene, and thus MIS and testosterone (mainly)

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52
Q

what does mullerian duct system develop into?

A

Fallopian tubes and uterus

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53
Q

what triggers development of mullerian duct system?

A

absence of testes, SRY gene, and thus MIS and testosterone (mainly)

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54
Q

what does lack of testosterone-derived DHT cause?

A

persistence of urogenital slit

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55
Q

t/f: embryonic ovaries secrete hormones that trigger development of external genitalia

A

false, vagina/female external genitalia development is not influenced by ovaries

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56
Q

what does androgen exposure during period of female genital development cause? and after 13th week of gestation?

A

development: develop male structures

after 13 weeks: female genitalia virilized (enlarged)

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57
Q

what is the process of male embryonic sexual development? (4)

A

SRY gene in embryonic germ cells produces TDF, which initiates differentiation of gonad medulla into a testis, interstitial/Leydig cells secrete testosterone which directs development of internal and external (DHT) genitalia, Sertoli cells secrete MIS which causes regression of Müllerian duct

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58
Q

What is the process of female embryonic sexual development?

A

lack of SRY gene causes differentiation into fetal ovaries, no MIS initiates internal genital development, no testosterone causes regression of Wolffian ducts and development external genitalia + vagina

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59
Q

what is androgen insensitivity syndrome?

A

impaired testosterone binding in XY genotype causes degeneration of mullerian ducts (MIS present) and Wollfian ducts (no testosterone activity), therefore are infertile

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60
Q

when is androgen insensitivity syndrome detected?

A

at puberty when menstrual cycle fails to initiate

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61
Q

what is congenital adrenal hyperplasia?

A

overproduction of androgens in fetus causes virilization of XX fetus and ambiguous genitalia

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62
Q

what causes androgen insensitivity syndrome?

A

mutation in androgen receptor gene

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63
Q

why is androgen insensitivity syndrome aka “testicular feminization”?

A

testes present but ext. female genitalia

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64
Q

what causes congenital adrenal hyperplasia?

A

mutation in cortisol gene synthesis causes incr ACTH and androgen production

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65
Q

what is a treatment for congenital adrenal hyperplasia?

A

cortisol replacement (normalizes ACTH but not ext. genitalia)

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66
Q

what is the general synthesis pathway for DHEA? where is it secreted?

A

cholesterol forms pregnenolone to form DHEA; adrenal cortex

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67
Q

what is the general synthesis pathway for estrone and estradiol? where are they secreted?

A

cholesterol forms pregnenolone to form progesterone which forms androstenedione that can be converted to estrone by aromatase or testosterone, aromatase converts testosterone to estradiol; ovaries

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68
Q

what is the general synthesis pathway for DHT?

A

cholesterol forms pregnenolone to form progesterone which forms androstenedione that is converted to testosterone, secreted by testes to target tissue where 5-a-reductase converts it to DHT

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69
Q

where is progesterone secreted in females?

A

ovaries

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70
Q

where are androgens synthesized? (2)

A

testes mainly but also adrenal cortex

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71
Q

t/f: androgens from the adrenal cortex are enough to sustain male reproduction functions

A

false, adrenal androgens are not potent enough

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72
Q

are adrenal androgens also secreted by women?

A

yes, from ovaries in small amounts

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73
Q

is DHT a more potent form of testosterone?

A

yes

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74
Q

what are estrogens vs estrogen?

A

estrogens: family of steroid hormones
estrogen: used interchangeably with estradiol

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75
Q

where are estrogens secreted from? (2)

A

ovaries and placenta

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76
Q

what is estradiol?

A

predominant estrogen in plasma

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77
Q

what individuals are estrone vs estriol mainly found in?

A

estrone: post-menopausal
estriol: pregnant women

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78
Q

where is estriol produced?

A

placenta

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79
Q

what are estrogens produced from? how?

A

androgens; aromatization

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80
Q

what enzyme is responsible for aromatization of androgens into estrogens?

A

aromatase

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81
Q

are estrogens found in males?

A

yes, released from testes

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82
Q

where are androgens converted to estrogens in males?

A

in non-gonadal tissues by aromatase

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83
Q

what is the HPG axis for sex hormones?

A

hypothalamus produces GnRH, GnRH stimulates ant pit to produce FSH and LH (gonadotropins), FSH and LH stimulate sex hormones

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84
Q

what can sex hormones do in HPG axis? (3)

A

stimulate gametogenesis, or any organ w/ a receptor, or negative feedback (or positive for females) on hypo (GnRH) ant pit (FSH and LH)

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85
Q

what cells secrete GnRH?

A

neuroendocrine cells in hypothalamus

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86
Q

t/f: impaired function of hypo/ant pit results in failure of gonads to secrete steroids/gametogenesis

A

true

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87
Q

what secretes progesterone in anatomical females?

A

ovaries and adrenal gland

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88
Q

what is the major secretory product of placenta during pregnancy?

A

progesterone (also during specific times during menstrual cycle)

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89
Q

t/f: progesterone is not present in males

A

false, progesterone is present in males as it’s a precursor/intermediate for adrenal steroids/androgens and estrogens

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90
Q

what is the action of gonadal steroids in a target cell?

A

diffuse into cells (lipid-soluble), bind to intracellular receptor to form complex, binds DNA in nucleus and modifies mRNA formation, protein synthesis, and circulating levels of protein

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91
Q

what are the 2 actions of gonadal steroids (not gametogenesis)?

A

development of accessory reproductive organs (ducts, breasts), and secondary sex characteristics (hair, body shape/height)

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92
Q

what does LH do in gonads? (2)

A

stimulates endocrine cells to produce steroid/sex and peptide hormones, stimulates gametogenesis in females

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93
Q

what does FSH do in gonads?

A

stimulates gametogenesis

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94
Q

in what scenarios does estrogen exhibit positive vs negative feedback in HPG axis?

A

positive: high levels of estrogen
negative: low to moderate levels

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95
Q

what is the pattern of secretion of GnRH?

A

pulsatile (every 1-3hrs)

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96
Q

is the pulsatile secretion of GnRH in males and femlaes?

A

yes

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97
Q

what hypothalamic region generates pulses of GnRH?

A

GnRH pulse generator

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98
Q

why is GnRH secreted in pulses?

A

steady, high levels of GnRH down-regulates GnRH receptors on gonadotropin cells, ant pit cant respond to GnRH

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99
Q

t/f: children with a GnRH deficiency can still mature sexually

A

false, GnRH deficiencies cause lack of sexual development (treated w/ PULSATILE GnRH)

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100
Q

what occurs directly after pulsatile GnRH secretion?

A

FSH and LH are stimulated/secreted

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101
Q

what is a clinical application of GnRH?

A

treatment for prostate/breast cancer (stimulates FSH/LH at first, then ant pit desensitizes)

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102
Q

what is kisspeptin?

A

peptide hormone critical in generating pulsatile secretion of GnRH

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103
Q

t/f: kisspeptin is essential for upstream mechanisms initiating timing of puberty

A

true

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104
Q

how can kisspeptin affect GnRH neurons?

A

can exhibit positive and negative feedback onto GnRH neurons from estrogen and sex steroids resp.

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105
Q

t/f: FSH and LH have different structures in each sex

A

false, same structure in each sex

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106
Q

what are inhibins?

A

peptides from gonads that affect ant pit

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107
Q

what are 4 enviro factors that can affect reproduction? (females > males)

A

stress, nutrition, day-light cycle (travelling, shift work, melatonin), environmental estrogens (endocrine disruptors)

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108
Q

what are 6 ex of enviro estrogens (endocrine disruptors)?

A

phytoestrogens (plants: soy), synthetics (plastic, pesticide, chemicals, pharmaceuticals: hormonal replacement/contraception)

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109
Q

what are 4 effects of enviro estrogens (endocrine disruptors)?

A

bind estrogen receptors and have positive or negative effects, accumulate in adipose, compromise gamete quality, disrupt developing embryos

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110
Q

where is the prostate?

A

encircles urethra

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111
Q

what is the effect of cancerous enlargement of the prostate?

A

impedes urination

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112
Q

where is the urethra in the penile shaft?

A

ventral side, surrounded by corpus spongiosum

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113
Q

what comprises the penile erectile tissue? (3)

A

corpus spongiosum, corpora cavernosa (2)

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114
Q

what is the glans?

A

tip of penis covered in foreskin (unless circumsized)

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115
Q

where are the testes located?

A

suspended outside abdomen in scrotum (2 sacs)

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116
Q

when do the testes descend from the abdomen?

A

7th month of pregnancy (w/ testosterone)

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117
Q

what is cryptorchidism? effect?

A

1 or both testes fail to descend and remain in abdomen; decr spermatogenesis but normal testosterone production

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118
Q

what does the spermatic cord do?

A

binds testicular blood vessels and nerves

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119
Q

why is vascular counter current exchange in the penis essential?

A

facilitates heat exchange btwn warm arterial and cool venous blood which maintains normal temp for spermatogenesis

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120
Q

t/f: normal testosterone production and secretion can occur at core body temp

A

true (not spermatogenesis)

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121
Q

where is the site of spermatogenesis?

A

seminiferous tubules in testicles

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122
Q

what encases bundles of seminiferous tubules?

A

outer fibrous capsule

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123
Q

what does the interstitial tissue of the testes feature?

A

blood vessels and Leydig cells

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124
Q

what does the spermatic cord pass through to get to testes?

A

inguinal canal

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125
Q

what do the seminiferous tubules converge into? (4 -> urethra)

A

sem. tubules -> rete testis -> efferent ductules -> epididymis -> vas deferens -> urethra

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126
Q

what are 4 of the contents and functions of accessory gland secretions?

A

nutrients (for sperm), protective buffers (neutralize acidic urine in male urethra and vaginal secretions), seminal vesicle chemicals (prostaglandins: incr motility?), mucus (lubrication)

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127
Q

where is mucus secreted from in male repro tract?

A

bulbourethral glands (for later semen passage)

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128
Q

what is another purpose for male secretions (other than sperm viability)?

A

protect from pathogens (antibacterial)

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129
Q

what is seminal plasma?

A

nonsperm portion of semen (99%)

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130
Q

what metal is present in semen?

A

zinc (unsure function)

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131
Q

how is a constant supply of undifferentiated sperm maintained?

A

one clone produced by each spermatogonium germ cell drops out to re-enter mitotic pathway (staggered development)

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132
Q

what occurs in the final phase of spermatid differentiation into sperm/spermatozoa?

A

cell remodelling and elongation

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133
Q

approx. how long does spermatogenesis take?

A

2 months

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134
Q

what surrounds each seminiferous tubule?

A

basement memb

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135
Q

what 2 types of cells are in the seminiferous tubule wall?

A

developing sperm and Sertoli

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136
Q

what is at the center of each seminiferous tubule?

A

lumen w/ mature sperm

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137
Q

where are the Leydig cells?

A

around/btwn seminiferous tubules in connective tissue

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138
Q

t/f: sperm-producing and testosterone-producing functions of the testes are carried out by the same structure

A

false, Leydig cells produce testosterone and sem tubules produce sperm (Sertoli cells)

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139
Q

t/f: Sertoli cells don’t require and can’t receive testosterone from Leydig cells

A

false, testosterone can freely diffuse into Sertoli cells and they require it

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140
Q

what is the “Sertoli-cell” barrier?

A

ring of Sertoli cells from basement memb to lumen of each sem tubule (blood testes barrier)

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141
Q

what are the 2 compartments of the sem tubule? what separates them?

A

basal and central; Sertoli ring

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142
Q

when are the Leydig cells quiescent vs active?

A

active in fetus, quiet after birth, reactive at puberty

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143
Q

what can Leydig cells also do w/ testosterone?

A

convert to estradiol w/ aromatase

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144
Q

what is the hormonal control of spermatogenesis? (5)

A

hypo releases GnRH, ant pit releases FSH and LH, LH stimulates Leydig cells to release test, test stimulates body for 2ndary effects and diffuses across blood-testis barrier into Sertoli cells, FSH stimulates Sertoli cells to produce cell products

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145
Q

what are 3 products of Sertoli cell stimulation?

A

inhibin (neg feedback of FSH), nourish developing sperm, androgen binding protein (ABP) (luminal secretions)

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146
Q

what is androgen binding protein (ABP)? purpose?

A

protein that binds Leydig-derived testosterone to cross Sertoli cell barrier into sem tubule lumen (allows high conc)

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147
Q

where does mitosis of sperm cells occur in sem tubule?

A

basal compartment btwn Sertoli cells

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148
Q

what occurs to defective sperm in sem tubule?

A

Sertoli cells phagocytose them

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149
Q

t/f: Sertoli cells produce chemical messengers in response to local testosterone

A

true, Leydig cells stimulate spermatogenesis and inhibin release (in Sertoli cells) via paracrine signals

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150
Q

when do sperm cells unbind from apical membrane of Sertoli cells?

A

when transformation is complete

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151
Q

where does final maturation of sperm occur?

A

epididymis

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152
Q

what occurs to sperm during final maturation in epididymis?

A

lose cytoplasm and develop tail

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153
Q

what are the 3 portions of a sperm cell?

A

head, midpiece, tail

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154
Q

what is the head of a sperm cell?

A

almost all nucleus, covered by acrosome

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155
Q

what does the acrosome contain?

A

protein-filled vesicle w/ enzymes necessary for fertilization

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156
Q

what is the midpiece of a sperm cell?

A

formed by mitochondria (E to move)

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157
Q

what is the tail of a sperm cell?

A

mostly flagellum (propels sperm)

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158
Q

what stores sperm until ejaculation?

A

vas deferens and epididymis

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159
Q

what prevents engorgement of epididymis? benefit?

A

fluid can be absorbed from lumen; concentrates sperm

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160
Q

what propels sperm to urethra during ejaculation?

A

peristaltic movements of vas deferens and epididymis

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161
Q

what is a vasectomy?

A

removal of segments from each vas deferens so sperm cant travel from epididymis

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162
Q

t/f: vasectomies result in fluid build-up

A

false, sperm break down and are reabsorbed

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163
Q

t/f: testosterone and Leydig cells are unaffected in a vasectomy

A

true

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164
Q

t/f: sperm production halts w/ a vasectomy

A

false

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165
Q

what is the passive process of sperm movement?

A

Sertoli cells produce secretions and incr P in sem tubule and push sperm as far as the epididymis (sperm not motile)

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166
Q

what are 8 factors that negatively affect sperm?

A

heat/P on scrotum, caffeine/nicotine/alcohol/marijuana, enviro toxins, hair growth stimulants/OTC drugs, laptops/phones (heat), saliva (acidic), lube/douche, estrogens in plastic (BPA)

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167
Q

how do estrogens in plasticizers (BPA) negatively affect male repro?

A

incr negative feedback in HPG axis which decr testosterone production

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168
Q

what 3 ways are negative effects exhibited by sperm?

A

decr sperm count, abnormal morphology, abnormal motility

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169
Q

what is the general process of penile erection? (6)

A

3 cylindrical compartments flaccid, sexual excitation, dilation of small arteries, incr BF and engorgement of vascular compartments, passive compression of adjacent veins (no outflow, maintains engorgement), erection

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170
Q

which ANS system and NT(s) are responsible for flaccid vs erect penis?

A

flaccid: sympathetic, NA/E (contract/vasoconstriction)
erect: parasymp, ACh and NO (relax/vasodilation)

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171
Q

what 2 processes must occur for vasodilation/relaxation in erection?

A

inhibition of sympathetic input, activation of non-adrenergic, non-cholinergic (NO, para) autonomic neurons to arteries

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172
Q

what are some primary stimuli (and pathway) for erection? (5, 4)

A

mechanoreceptors in penis, higher brain centre input such as thoughts, emotions, sights, and odours -> incr afferent neuron firing -> (lower) spinal reflex -> changed efferent neural outflow

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173
Q

what is ejaculation?

A

spinal reflex that discharges semen w/ stimulation of penile mechanoreceptors

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174
Q

what is the 1st phase of ejaculation?

A

emission: sympathetic activity contracts epididymis, vas def, ejaculatory ducts, prostate and seminal vesicles, moving semen into urethra

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175
Q

what is the 2nd phase of ejaculation?

A

ejaculation: semen expelled from urethra by contractions of urethral smooth muscle and skeletal muscle at base of penis

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176
Q

what prevents retrograde ejaculation?

A

closure of sphincter at base of bladder during ejaculation phase

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177
Q

what is an orgasm? what follows it?

A

muscular contractions, pleasure and systemic physiological changes (incr HR, BP) that is followed by a latent/ref period (no erection possible)

178
Q

what is erectile dysfunction (ED)?

A

consistent inability to achieve/maintain an erection sufficient for penetration (not called impotence anymore)

179
Q

when is ED most common?

A

40-70 yrs old (>10%)

180
Q

what are 5 other causes (not nerve/vasc. impairment) of ED?

A

endocrine disorders (decr test), drug use, alcohol, diseases, psych factors (stress/trauma)

181
Q

what is the most common cause of ED?

A

damage/impairment of efferent nerves that control vasculature (needed for erection)

182
Q

what are 3 drug treatments for ED?

A

NO supplementation, PDE5 inhbitors, Alprostadil

183
Q

how does NO supplementation treat ED? (3)

A

NO incr GMP -> cGMP in smooth muscle cell, which decr Ca and causes smooth muscle relaxation/vasodilation

184
Q

how do PDE5 inhibitors treat ED? (3)

A

PDE5 breaks down cGMP so inhibition incr cGMP in smooth muscle cell, which decr Ca and causes smooth muscle relaxation/vasodilation

185
Q

how does Alprostadil treat ED? (3)

A

activates prostaglandin E (PGE1) receptors which incr ATP -> cAMP in smooth muscle cell, which decr Ca and causes smooth muscle relaxation/vasodilation

186
Q

what occurs to testosterone in the prostate vs brain, liver, and adipose?

A

prostate: conversion to DHT by 5 a-reductase

brain/liver/adipose: conversion to estradiol by aromatase

187
Q

what does a deficiency in 5 a-reductase and aromatase suggest?

A

testosterone deficiency

188
Q

t/f: androgens don’t mediate libido

A

false, they do

189
Q

what are functions of DHT (4) vs estradiol (2) vs testosterone (6) in males?

A

DHT: facial/body hair, acne, scalp hair loss, prostate growth

estradiol: bone formation, breast tissue
testosterone: muscle mass, skeletal growth, spermatogenesis, sexual function, libido, erection

190
Q

what is a possible treatment for prostate cancer and male pattern baldness?

A

5 a-reductase inhibitors (decr DHT) but can neg affect fertility

191
Q

what are 4 effects of decr testicular function/testosterone synthesis from castration or drugs?

A

decr size of accessory organs, decr secretion from glands (decr semen, sperm viability), decr smooth muscle activity of ducts (decr ejac.), decr sex drive/erection

192
Q

what is a treatment for decr testicular function/testosterone synthesis?

A

testosterone treatment

193
Q

when does puberty occur in males?

A

12-16 yrs old

194
Q

how are first signs of male puberty detected?

A

secretion of adrenal androgens (not gonadal)

195
Q

what stimulates first signs of male puberty?

A

ACTH from ant pit (stimulates adrenal glands)

196
Q

what occurs during the first stages of male puberty?

A

development of pubic and auxiliary hair, beginning of growth spurt (mitigated by adrenal androgens)

197
Q

after first stages (stimulated by adrenal androgens), what controls other events in male puberty?

A

HPG axis

198
Q

what are 2 hypothesized initiators of male puberty?

A

decr sensitivity of brain to neg feedback of gonadal hormones (low secretion), incr spontaneous activity of kisspeptin neurons in hypo

199
Q

what is the general process of male puberty? (5)

A

possible initatiors (kisspeptin neurons), incr activity (f and conc.) of GnRH, incr ant pit gonadotropins, stimulate sem tubules and testosterone secretion, 2ndary sex characteristics/accessory organs/sex drive)

200
Q

what is growth of 2ndary male characteristics dependent on?

A

DHT and testosterone

201
Q

what are 6 ex of male 2ndary sex characteristics?

A

growth of larynx, thick skin oil gland secretions, masculine fat distribution, androgen-stimulated bone growth, androgen-stimulated muscle growth, androgen-stimulated erythropoietin secretion from kidneys

202
Q

what stimulates and terminates male bone growth in puberty?

A

androgens via GH secretion; testosterone stimulates closure of epiphyseal plates

203
Q

what is the effect of androgen-stimulated erythropoietin secretion from kidneys in male puberty?

A

incr hematocrit in males (incr RBCs)

204
Q

What are 2 positive and 3 negative effects of using synthetic androgens?

A

Pos: incr muscle mass and athletic performance
Neg: overstimulation of prostrate, aggression, decr GnRH, LH and FSH

205
Q

Why is decr GnRH, LH, and FSH from using synthetic androgens problematic? (3)

A

Decr endogenous testosterone production and spermatogenesis in Sertoli cells, decr testicular size and sperm count, addictiveness (brain function?)

206
Q

how do synthetic androgens decr endogenous testosterone production?

A

through neg feedback on GnRH and gonadotropins (can’t cross blood-testis barrier)

207
Q

What is a possible male birth control pill?

A

Low dose anabolic steroids (decr fertility but other neg side effects)

208
Q

What is hypogonadism?

A

Decr testosterone release from testes

209
Q

What’s the diff btwn primary and secondary hypogonadism?

A

Primary: caused by testicular failure
Secondary: caused by decr stimulation of testes by LH/FSH or GnRH (disorder w/ hypo/ant pit)

210
Q

What is the effect of having hypogonadism before puberty?

A

Failure to develop secondary sex characteristics and normal sperm

211
Q

What is an ex of a primary cause of hypogonadism?

A

Klinefelter’s syndrome (genetic: XXY)

212
Q

What causes Klinefelter’s syndrome?

A

Failure of chr to separate during meiosis (in parents)

213
Q

How does Klinefelter’s syndrome present itself? (4)

A

Before puberty: normal
After puberty: small, poorly developed testes (decr Leydig and Sertoli cell function), absence of 2ndary sex characteristics, incr breast size, high FSH/LH

214
Q

What is the effect of having decr Leydig and Sertoli cell function in Klinefelter’s syndrome? (3)

A

Poor Leydig function: decr [testosterone] -> abnormal sem tubule development, decr sperm production

215
Q

What is the cause of having high LH/FSH in Klinefelter’s syndrome?

A

Loss of inhibin and androgen neg feedback

216
Q

What is a treatment for Klinefelter’s syndrome?

A

Androgen replacement therapy

217
Q

What are 3 causes of secondary hypogonadism?

A

Hyperprolactinemia, hypopituitarism, GnRH deficiency

218
Q

What is hyperprolactinemia and how does it cause secondary hypogonadism?

A

Secretion of prolactin from pituitary gland cells (lactotrophs, tumour?); inhibits LH and FSH secretion from ant pit (paracrine)

219
Q

What is hypopituitarism and how does it cause secondary hypogonadism?

A

Loss of ant pit function (head trauma, infection/inflammation), decr secretion of LH and FSH

220
Q

What are 3 possible treatments for hypopituitarism?

A

Testosterone replacement, cortisol, thyroid hormone

221
Q

What are 3 effects of male castration in adulthood?

A

Same 2ndary sex characteristics, decr androgen sensitive tissues, decr size of accessory ducts and testes

222
Q

What is andropause?

A

Steady decr in testosterone levels at ~40yrs (not as drastic as menopause)

223
Q

What causes andropause? (2)

A

Deterioration of testicular function, failure of gonads to respond to ant pit gonadotropins (decr sensitivity to LH/FSH)

224
Q

What are 3 effects of andropause?

A

Decr libido, decr sperm motility/viability, depression

225
Q

T/f: males stop being fertile after andropause

A

False, sperm production does not decr immediately w/ testosterone decr (remain fertile for years afterwards but then decr)

226
Q

What are fallopian tubes aka?

A

Oviducts

227
Q

What is at the end of each oviduct (not uterus)?

A

Fimbrea (brush over ovaries)

228
Q

What are the components of the female internal genitalia?

A

2 ovaries, 2 oviducts, 1 uterus, cervix, and upper portion of vagina

229
Q

What is the female external genitalia collectively referred to as?

A

Vulva

230
Q

What are the components of the female external genitalia?

A

Mons pubis (fatty tissue at top), labia majora, labia minora, clitoris, vaginal vestibule (opening), vestibular glands

231
Q

What are the female analogues to the male penis and scrotum?

A

Penis-clitoris

Scrotum-labia majora

232
Q

What is the hymen?

A

Thin fold of mucous memb that partly overlies vaginal vestibule (considered ext genitalia)

233
Q

What are 4 main functions of the ovaries?

A

Fetal oogenesis, oocyte maturation (birth), ovulation (puberty), sex hormone secretion (endocrine function)

234
Q

What 3 sex hormones are secreted from the ovaries?

A

Estrogen, progesterone, inhibin

235
Q

What is considered endocrine tissue in the ovaries?

A

Corpus luteum (differentiated eggless follicle)

236
Q

Where do ova/eggs exist in the ovaries?

A

In follicles

237
Q

What are the 5 stages of ova development?

A

Primordial follicle, primary follicle, preantral follicle, early antral follicle, mature/Graafian follicle

238
Q

When can primordial follicles progress into preantral and early antral stages?

A

Throughout infancy, childhood, and menstration (not just after puberty)

239
Q

What is the structure of the primordial follicle?

A

Primary oocyte surrounded by granulosa cells

240
Q

What do granulosa cells secrete?

A

Estrogen, progesterone and inhibin

241
Q

What is the structure of the primary follicle?

A

Fully grown oocyte separated from granulosa cells by zona pellucida

242
Q

What does the zona pellucida contain? why?

A

Glycoproteins; help w/ fertilization by binding sperm to egg surface (after ovulation)

243
Q

What is the structure of the preantral follicle?

A

Oocyte surrounded by multiple layers of granulosa cells, has early theca cells

244
Q

What is the antrum? When and how is it generated?

A

Fluid-filled space; in early antral follicle by granulosa cells

245
Q

What is the theca?

A

Differentiated connective tissue (ovarian stroma) around granulosa cells that synthesizes estrogen

246
Q

How do theca cells work w/ granulosa cells to produce estrogen?

A

Theca cells secrete androgens in response to LH, which diffuse into granulosa cells which respond to FSH and convert them to estrogen (via aromatase)

247
Q

How do inner granulosa cells associate w/ and support oocyte?

A

Form gap junctions via cytoplasmic process and can exchange nutrients and chemical messengers

248
Q

What is the structure of the Graafian follicle? (3 major contents)

A

Mature follicle w/ cumulus oophorus, many layers of theca cells, and large antrum (allows major enlargement)

249
Q

What is the cumulus oophorus?

A

Extension of granulosa cells that surround oocyte (to separate from rest of follicle) “egg on a cloud”

250
Q

What occurs to 99.99% of ovarian follicles present at birth?

A

Atresia (breakdown)

251
Q

What occurs to follicles at beginning of menstrual cycle?

A

cohort of ~10-25 preantral and early antral follicles develop into larger antral follicles

252
Q

What occurs to follicles in the 1st week of menstrual cycle?

A

Largest antral follicle from cohort is selected to develop further and non-dominant follicles undergo atresia

253
Q

How is the dominant follicle selected?

A

By local estrogen secretion (has most granulosa cells to respond to FSH and secrete estrogen)

254
Q

What occurs to the Graafian follicle at ovulation? (5)

A

Emerges from meiotic arrest to undergo 1st meiotic division to 2ndary oocyte, cumulus separates from follicular wall (floats in antral fluid), follicle physically distends from surface of ovary, thin wall btwn follicle and ovary rupture (enzymatic digestion), P from antral fluid pushes 2nday oocyte (surrounded by zona pellucida, gran cells, cumulus) onto ovarian surface

255
Q

T/f: if more than one folllicle reaches maturity, multiple eggs can be ovulated

A

True, multiple births -> fraternal twins (different sperm)

256
Q

how is the corpus luteum formed?

A

after mature follicle discharges egg+antral fluid, remaining granulosa cells enlarge (change pheno)

257
Q

what does corpus luteum secrete (endocrine)?

A

estrogen, progesterone and inhibin

258
Q

what occurs to the corpus luteum if fertilization does not occur? (2)

A

degenerates by apoptosis to form corpus albicans, loses endocrine function which initiates menstruation (max development ~10 days)

259
Q

what are 2 phases of menstrual cycle (ovarian)? separated by?

A

follicular and luteal; ovulation

260
Q

what occurs during the follicular vs luteal phases (ovarian)?

A

follicular: mature follicle and 2ndary oocyte develop
luteal: formation of corpus luteum (until degen wo/ fertilization)

261
Q

how do hormone patterns during menstrual cycle regulate ovarian/HPG events? (1st week: 2, 2nd week: 5, before ov: 3, ov: 1, luteal: 4)

A

1st week: low estrogen (loss of corpus luteum) causes incr LH and FSH (decr -FB), low prog
2nd week: multiple follicles develop, incr estrogen, FSH decr (est -FB), non-dom follicles degenerate, low prog
before ovulation: incr est now has +FB, estrogen decr, slight prog incr
during ovulation: LH surge (est +FB)
luteal: corpus luteum incr estrogen and prog, decr LH/FSH (-FB), est/prog decr rapidly wo/ fertilization, LH/FSH incr

262
Q

t/f: LH and prog levels are somewhat stable during the follicular phase

A

true

263
Q

What hormone receptors do granulosa vs theca have at first vs later in menstraul cycle?

A

Gran: at first: only FSH, later: FSH and LH
Theca: only LH (never FSH)

264
Q

What stimulates multiplication, estrogen production and secretions for antrum in granulosa cells?

A

FSH (estrogen can exhibit further +FB)

265
Q

What male cells are the female counterparts for theca and granulosa cells?

A

Granulosa: Sertoli (germ cell enviro, stim by FSH/sex H)
Theca: Leydig (produce androgens, stim by LH)

266
Q

How does the dom foll have incr sensitivity to FSH when it decr in 2nd week of menstrual cycle?

A

Has incr FSH receptors

267
Q

T/f: FSH and LH stimulation of the dom foll is enough to produce estrogen to support incr plasma conc in 2nd week of menstrual cycle

A

True

268
Q

What does estrogen have -FB on?

A

Ant pit: decr FSH and LH (in response to GnRH)

Hypo: decr amplitude of GnRH pulses and total secreted

269
Q

What decr more from estrogen -FB? Why?

A

FSH > LH; inhibin (from granulosa cells) primarily inhibits FSH

270
Q

how long does estrogen peak last in the late follicular phase?

A

1-2 days

271
Q

how could GnRH incr during the estrogen peak? (2)

A

+FB on hypothalamus directly (incr GnRH) or activate kisspeptin neurons (upstream of GnRH)

272
Q

t/f: estrogen +FB is necessary for normal menstrual cycles and ovulation

A

true

273
Q

what accounts for the decr in estrogen and slight incr in progesterone right before ovulation?

A

granulosa cells decr estrogen and begin to release progesterone

274
Q

what are 7 functions of granulosa cells?

A

nourish oocyte, secrete chem messengers to oocyte and theca cells, secrete antral fluid, follicle development via estrogen and FSH in early/middle follicular phase, convert androgens to estrogen via aromatase, secrete inhibin to inhibit FSH, react to LH for ovulation and conversion to corpus luteum

275
Q

what stimulates conversion of theca and granulosa cells into corpus luteum?

A

drop in LH (after surge)

276
Q

how long does the corpus luteum function for?

A

10-14 days

277
Q

what does the corpus luteum secrete?

A

estrogen, progesterone, inhibin

278
Q

what does progesterone from corpus luteum do? (2)

A

inhibits gonadotropins (through ant and hypo), and prevents LH surge in luteal phase

279
Q

t/f: plasma gonadotropin levels are high in the luteal phase

A

false they are low (don’t want to waste energy stimulating follicle when ovulation has already occurred)

280
Q

what is day 1 of the menstrual cycle?

A

first day of menstrual flow

281
Q

what occurs during the menstrual phase (uterine)? (2)

A

bleeding, degeneration of endometrium

282
Q

what occurs during the proliferative phase (uterine)?

A

growth of endometrium and myometrium w/ incr estrogen (from developing follicle - overlap w/ follicular phase)

283
Q

when is the proliferative phase?

A

between cessation of menstruation and ovulation (~10 days)

284
Q

what occurs during the secretory phase (uterine)? (6)

A

endometrium converts to secretory tissue (changes pheno) in response to progesterone from corpus luteum, glands become coiled, highly vascularized, accumulate enzymes, and secretes glycogen (in glandular epithelium), then secretes glycoproteins and mucopolysaccharides (primes endometrium for possible implantation)

285
Q

when is the secretory phase?

A

after ovulation until next period

286
Q

What ovarian phases correspond to what uterine phases?

A

Follicular: menstrual and proliferation
Luteal: secretory

287
Q

What induces expression of progesterone receptors on endometrial cells in proliferative phase?

A

Incr estrogen levels

288
Q

Why is it important for endometrium to begin expressing progesterone receptors in the proliferative phase?

A

So it can respond to progesterone in secretory phase and become secretory tissue

289
Q

What are 2 functions of progesterone?

A

Inhibits myometrial contractions and opposes stimulatory actions and estrogen + prostaglandins

290
Q

Why is progesterone needed to inhibit myometrial contractions and oppose estrogen/prostaglandins?

A

Ensures safe implantation and maintains uterine ‘quiescence’ (prevents premature birth)

291
Q

What could be a reason for recurrent miscarriages?

A

Low progesterone

292
Q

What modulates production and consistency of cervical mucous?

A

Sex hormones

293
Q

How, when and why does estrogen affect cervical mucous?

A

Makes it abundant, watery, and clear during ovulation to facilitate sperm movement

294
Q

How, when, and why does progesterone affect cervical mucous?

A

Makes it thick and sticky after ovulation to form a plug that protects uterus and embryo from bacteria (and further sperm if fertilization already occurred)

295
Q

What is involution of the corpus luteum?

A

Degeneration of corpus luteum if fertilization does not occur

296
Q

What are 3 effects of corpus luteum involution?

A

Decr estrogen and progesterone, loss of hormonal support for endometrium, menstruation (day 28 to 1)

297
Q

What are 4 events in menstruation?

A

Construction of uterine blood vessels, disintegration of uterine lining, rhythmic contractions of uterine muscle, dilation of endometrial arterioles

298
Q

What causes uterine blood vessels to constrict during menstruation?

A

Prostaglandins produced by endometrium in response to decr estrogen and progesterone (inhibit prostaglandins)

299
Q

What is the purpose of constricting uterine blood vessels during menstruation?

A

Deprives endometrial cells of O2 and nutrients

300
Q

What causes rhythmic contractions of uterine smooth muscle?

A

Overproduction of prostaglandins

301
Q

What causes dysmenorrhea and systemic symptoms (GI issues) during menstruation?

A

Overproduction of prostaglandins (constrict blood vessels and contractions)

302
Q

What is disintegrated during menstruation?

A

All but a thin, base layer to regenerate endometrium for next cycle

303
Q

What cause dilation of endometrial arterioles during menstruation?

A

Previous hypoxia (from constriction) causes incr CO2 and dilation

304
Q

What causes hemorrhage through endometrial capillary walls? Effect?

A

Dilation of endometrial arterioles; expulsion of blood and endometrial tissue through vagina

305
Q

how do hormone patterns during menstrual cycle regulate uterine/HPG events? (1st week: 3, 2nd week: 3, 3rd week: 3, 4th week: 3)

A

1st week: decr est and prog (corpus luteum degenerates), uterine lining sloughs, incr LH and FSH
2nd week: est incr (dom foll), endometrium develops, cervical mucous clear and watery
3rd week: corpus luteum secretes est and prog, endometrium becomes secretory, cervical mucous thick and sticky
4th week: corpus luteum involution, est and prog decr, endometrium sheds

306
Q

How does estrogen exhibit “pro-progesterone” effects? (Estrogen priming)

A

Incr synthesis of progesterone receptors in tissues (including endometrium) and thus responsiveness to progesterone

307
Q

What does a peak in progesterone suggest?

A

Ovulation occurred (incr basal body temp, inhibits vaginal cell proliferation)

308
Q

How does progesterone exhibit “anti-estrogen” effects?

A

Decr estrogen receptors (for uterine “quiescence”)

309
Q

what is the only direct measure of ovulation?

A

Clinical pregnancy confirmation (incr basal body temp is indirect/neural)

310
Q

What is a difference btwn female and male puberty?

A

Female initiates earlier (10-12 y/o)

311
Q

What is leptin? and how does it play a role in female puberty?

A

an adipokine (hormone from fat); stimulates GnRH production

312
Q

how do low GnRH, gonadotropins, and estrogen (strong -FB) affect female characteristics before puberty? (4)

A

no follicle maturation beyond early antral stage, no menstrual cycle, accessory organs remain small and non-functional, minimal secondary sex characteristics

313
Q

what is amenorrhea?

A

failure to have menstrual flow/menses

314
Q

what is primary vs secondary amenorrhea?

A

1’: failure to initiate menarche

2’: loss of previously normal menstrual cycles

315
Q

what are some causes for primary vs secondary amenorrhea?

A

1’: anorexia nervosa (body fat/leptin?)

2’: pregnancy, menopause, anorexia nervosa

316
Q

how does female athleticism affect their sex characteristics? 4 effects?

A

exercise considered a stressor that inhibits the HPG axis; pre-pubertal appearance, minimal body fat (decr leptin?), hypogonadism, possibly amenorrhea (if consistent)

317
Q

what is the optimal time frame for fertilization?

A

5 days before and 1 day after ovulation

318
Q

why is the optimal time for fertilization 5 days before and 1 day after ovulation?

A

sperm are viable for 4-6 days after ejaculation (can stay in female repro tract) and ovum is only viable 24-48 hours after ovulation (key limiting factor)

319
Q

what is capacitation?

A

removal of cholesterol, carbs, and proteins from sperm head after several hours in female repro tract (its secretions) that is necessary for sperm’s ability to fertilize

320
Q

how does capacitation affect sperm? why? (2)

A

changes wave-like to whip-like tail movements (incr propulsion) and alters pmemb (incr fusion w/ egg pmemb)

321
Q

where and when does fertilization occur?

A

in fallopian tube; 24-48 hours after ovulation

322
Q

what do the many sperm cells move between to try and fertilize egg?

A

corona radiata (layers of granulosa cells around egg)

323
Q

what do sperm bind to on egg?

A

zona pellucida

324
Q

what does zona pellucida contain that binds to sperm?

A

glycoproteins that act as sperm receptors (proteins exposed w/ capacitation)

325
Q

what does sperm binding to zona pellucida trigger?

A

acrosome reaction

326
Q

where does the acrosome reaction occur?

A

in bound sperm

327
Q

what is the acrosome reaction?

A

alteration of sperm pmemb which exposes acrosomal enzymes to zona pellucida, enzymes digests zona and allows sperm to advance w/ tail movements

328
Q

what is the “race against time”?

A

many sperm compete to reach egg and fuse both pmembs

329
Q

what part of the sperm enters egg cytosol?

A

head (midpiece and tail can enter but are destroyed)

330
Q

what is the “block to polyspermy”?

A

prevention of multiple sperm fertilizing an egg to preserve zygote viability (can occur - abnormal)

331
Q

how is “block to polyspermy” ensured?

A

w/ the cortical reaction (changes membrane potential when egg and sperm pmembs fuse)

332
Q

what is the cortical reaction?

A

fusion of 1st sperm w/ egg releases cortical granules (cytosolic secretory vesicles) into space btwn egg pmemb and zona pellucida, enzymes in granules enter and harden zona pellucida which inactivates further sperm binding (are released/rejected)

333
Q

t/f: many sperm can undergo acrosome reaction

A

true, fusion of one w/ egg pmemb causes fertilization

334
Q

what are the steps to embryogenesis after fertilization? (6)

A

egg completes second meiotic division hours after fertilization, 2nd polar body extruded and disintegrates, DNA of pronuclei (23 chr of egg and sperm) replicated, pronuclear pmembs degenerate, pronuclei fuse, cell prepared for mitosis (completes fertilization and zygote formation)

335
Q

what occurs to the ovulated egg if fertilization did not occur?

A

egg degenerates and is phagocytosed by cells lining the uterus, lost w/ menses (doesn’t complete 2nd meiotic division)

336
Q

how long is the conceptus housed in the fallopian tubes? Why

A

3-4 days; contains nutrients important for conceptus viability

337
Q

what ensures the conceptus stays in the fallopian tube for a few days after fertilization?

A

estrogen causes contraction of smooth muscle at junction btwn fallopian tube and uterus

338
Q

what allows conceptus to move to uterus?

A

incr plasma progesterone levels relax smooth muscle btwn fallopian tube and uterus (opposes estrogen)

339
Q

t/f: cell undergoes multiple meiotic division in fallopian tube wo/ any change in overall size

A

true, 16-32 cell conceptus reaches uterus approx. same size as fertilized egg

340
Q

how long does conceptus float freely in intrauterine fluid? Why?

A

~3 days; fluid has nutrients

341
Q

t/f: conceptus undergoes cell division up to 100 cells in uterine fluid and enters blastocyst stage

A

true

342
Q

what is a feature of the blastocyst stage?

A

cells of conceptus are no longer totipotent (undergo differentiation)

343
Q

what are 3 parts of the blastocyst?

A

trophoblast (outer cell layer), inner cell mass (gives rise to human), central fluid-filled cavity

344
Q

t/f: trophoblast surrounds the embryo and fetus throughout development

A

true

345
Q

what does the trophoblast do? (2)

A

contributes nutrition and hormone secretion

346
Q

when is the blastocyst stage w/ in the menstrual cycle?

A

day 14-21 (luteal/secretory)

347
Q

when does the blastocyst implant into the endometrium?

A

day 21 (7 days after ovulation)

348
Q

what is the orientation of the blastocyst when it embeds in the endometrium?

A

has cell mass towards endometrium

349
Q

what allows the blastocyst to implant?

A

stickiness of trophoblast cells

350
Q

what provides metabolic fuel and raw materials to embryo for first few weeks after implantation?

A

endometrial cells

351
Q

what is placentation?

A

formation of placenta by interlocking fetal and maternal tissues

352
Q

what is the purpose of the placenta? (3)

A

takes over embryonic and eventual fetal nutrition (after endometrium), oxygenation, and waste removal (site of exchange)

353
Q

what are the 3 portions of the placenta?

A

embryonic (chorion), chorionic villi, maternal (endometrium)

354
Q

What is the chorion?

A

Outer layer of trophoblast cells (embryo)

355
Q

What are the chorionic villi?

A

Rich capillary network that is part part of embryonic circulation and projects into endometrium

356
Q

t/f: there is mixing of maternal and fetal blood in chorionic villi

A

False

357
Q

What do chorionic villi secrete? Why?

A

Enzymes and paracrine factors that alter endometrium; creates pockets in endometrium for blood exchange

358
Q

What are pockets in endometrium filled w/ maternal arteriole blood that surround each chorionic villi called?

A

Sinus

359
Q

What forms the amnion/amniotic sac?

A

inner cell mass

360
Q

What is the amnion/amniotic sac?

A

epithelial lining

361
Q

Where is the amniotic cavity?

A

Between inner cells mass and chorion

362
Q

What does the amnion fuse with?

A

Inner surface of chorion

363
Q

What is the fetal ECF? (when amnion fuses w/ chorion)

A

Amniotic fluid

364
Q

What are 3 purposes of amniotic fluid?

A

Buffers mechanical disruption, temperature fluctuations, prevents dehydration

365
Q

What state is the fetus in for last 8 months of pregnancy?

A

Free-floating in amniotic fluid, attached to placenta by umbilical cord

366
Q

What are the hormonal changes throughout pregnancy?

A

Estrogen and progesterone continue to increase throughout pregnancy

367
Q

What are the functions of estrogen and progesterone during pregnancy? (2, 2)

A

Est: stimulates growth of uterine muscle, supplies contractile force for parturition
Prog: inhibits uterine contractility (opposes estrogen) and prevents premature delivery

368
Q

What produces most of the estrogen and progesterone during first 2 months of pregnancy?

A

Corpus luteum

369
Q

What maintains the corpus luteum during pregnancy?

A

Human chorionic gonadotropin (hCG)

370
Q

What secretes hCG at endometrial invasion stage?

A

Trophoblast cells

371
Q

T/f: hCG produced by trophoblast cells is enough to be detected in moms plasma/urine by a pregnancy test

A

True

372
Q

How can a pregnancy test give a false positive?

A

If test was taken too early (hCG not high enough)

373
Q

T/f: placenta has enzymes needed for progesterone synthesis during 2nd and 3rd trimester

A

true

374
Q

How does placenta produce estrogen during 2nd and 3rd trimesters? (3)

A

Since it doesn’t have enzymes to synthesize androgens, gets androgens from ovaries/adrenal glands/fetal adrenal glands, then can convert to estrogen w/ aromatase

375
Q

What is parturition?

A

Childbirth

376
Q

How long is a full term human pregnancy?

A

40 weeks

377
Q

When is a pregnancy term started from?

A

First day of last menstrual cycle (2 weeks before conception)

378
Q

How many weeks from ovulation and conception does a full term childbirth occur?

A

38 weeks

379
Q

When does parturition occur? What does it culminate in?

A

Final weeks of pregnancy; delivery of baby and placenta

380
Q

What maintains integrity of cervix (firmness) and loose connections of myometrial smooth muscle cells (SMCs) during pregnancy?

A

Progesterone

381
Q

What does incr in estrogen (» prog) do late in pregnancy? (3)

A

Softens cervix, connect SMCs (via connexins), expresses oxytocin receptors on myometrium

382
Q

What is the purpose of SMCs connexins towards end of pregnancy? (Via est)

A

Permits coordinated contractions of smooth muscle

383
Q

What does cervix softening, SMC connexins, and myometrial oxytocin Rs via est late pregnancy ensure?

A

Strong, rhythmic contractions of myometrium

384
Q

When do mini contractions begin? Aka?

A

Week 30; Braxton Hick’s

385
Q

T/f: Braxton Hick’s contractions move the fetus though female repro tract

A

False

386
Q

What occurs to the fetus in the final month of pregnancy?

A

Move downwards in contact w/ cervix (and other uterine contents)

387
Q

What are 7 steps of labour and delivery?

A

Amniotic sac ruptures (enzymatic breakdown), amniotic fluid flows out of vagina, powerful uterine contractions (10-15 min intervals then shorten), cervix dilated and forced open (max. 10cm), contractions move fetus through cervix and vagina (bearing down incr P), delivery and constriction of umbilical and placental vessels, placental delivery

388
Q

T/f: medical intervention is usually needed during labour and delivery

A

False, usually it isn’t unless forceps or C-section is required

389
Q

What position are 90% of births in?

A

Baby is head-first

390
Q

What are 4 controllers of parturition?

A

Properties of myometrium, uterine prostaglandin secretion, oxytocin, progesterone (during pregnancy)

391
Q

How do properties of myometrium control parturition?

A

SMCs have auto rhythmic response to fetal stretch (reflex contraction)

392
Q

How does uterine prostaglandin secretion control parturition?

A

Stimulates smooth muscle contraction

393
Q

How does oxytocin stimulate parturition?

A

Stimulates uterine muscle to incr contractility and prostaglandin synthesis (incr oxytocin Rs from previous est incr)

394
Q

Where and how is oxytocin released?

A

Reflex secretion from posterior pituitary in response to cervical stretch

395
Q

How does progesterone control parturition?

A

DURING PREGNANCY, prog decr uterine contractions by decr myometrial sensitivity to estrogen, oxytocin and prostaglandins

396
Q

T/f: progesterone withdrawal does not occur in humans

A

True

397
Q

What is the positive feedback mechanism in parturition? (5) how does it stop?

A

As baby drops lower in uterus to initiate labour, incr cervical stretch (hypo input) stimulates oxytocin release, incr uterine contractions, pushes baby against cervix which incr cervical stretch; delivery stops cervical stretch input to hypo

398
Q

What is lactogenesis?

A

Lactation, production, and secretion of milk by mammary glands

399
Q

What occurs to mammary glands during pregnancy?

A

Incr in size and number

400
Q

What is the site of milk secretion?

A

Alveoli (converge into nipples)

401
Q

What are 2 cells and diff functions in breast alveoli?

A

Epithelial cells: responsible for milk secretion (line inner surface of alveoli)
Myoepithelial: contractile cells that deliver milk (around alveoli)

402
Q

What hormone stimulates milk production?

A

Prolactin

403
Q

Why is there no milk secretion during pregnancy if there is high prolactin, large and developed breasts?

A

Very high levels of estrogen and progesterone inhibit action of prolactin at mammary glands

404
Q

What releases milk production from estrogen and progesterone inhibition during pregnancy?

A

Delivery of placenta removes source of estrogen and progesterone so prolactin can now act on mammary glands to stimulate milk production

405
Q

How is milk production maintained (PRL and OXY) during breastfeeding? (5)

A

Suckling stimulates nipple mechanoreceptors, input to hypo for incr PRF/H and oxytocin (post pit) release, PRF/H stimulates prolactin release from ant pit, prolactin stimulates mammary epithelial cells to incr milk synthesis, oxytocin stimulates contraction of myoepithelial cells around alveoli to eject milk

406
Q

What is the “milk ejection reflex”/“milk letdown”?

A

Contraction of myoepithelial cells w/ OXY stimulation to eject milk from alveolar lumen into ducts (secreted into lumen w/ PRL)

407
Q

How do higher brain centres exhibit effects on milk ejection reflex?

A

Nursing mother can eject milk by hearing baby’s cry or thinking about nursing (reflex OXY secretion from post pit)

408
Q

What is colostrum?

A

Watery, protein-rich fluid that is the first substance secreted from breasts after delivery

409
Q

What is in colostrum? Purpose?

A

Antibodies and leukocytes that mediate newborns immune system (required for LT activation)

410
Q

What are 9 components of breast milk?

A

Water, proteins, lipids, lactose (carb), minerals, vitamins, Abs/WBCs, hormones (growth factors), NTs (opioids)

411
Q

What is the purpose of growth factors/hormones in breast milk?

A

Aid tissue development and maturation in newborn

412
Q

What is the purpose of neuropeptides/endogenous opioids in breast milk?

A

Shapes infants brain and behaviour

413
Q

What ensures newborn does not denatures proteins consumed in breast milk?

A

Low gastric acidity (higher pH)

414
Q

What ensures newborn absorbs proteins in breast milk?

A

Intestinal epithelium more permeable to proteins (vs adult)

415
Q

T/f: all components of breast milk are from mom’s circulation

A

False, some synthesized by breast tissue and transported from maternal blood to milk

416
Q

What else can be passed through breast milk? (3)

A

Infectious agents (HIV), drugs and alcohol

417
Q

What is contraception?

A

Birth control methods that work before implantation (preventative)

418
Q

T/f: abortion is considered contraception

A

False, is not considered preventative (reactive)

419
Q

Where do oral contraceptives, IUDs vs barrier devices (condom) target?

A

Oral: ovaries
IUD: uterus
Condom: cervix

420
Q

What are 8 ex of contraceptives?

A

Vasectomy, condom, tubal ligation, vaginal diaphragm, vaginal cap, spermicides, IUD, birth control pills

421
Q

What is abortion?

A

Death of embryo or fetus after implantation

422
Q

What are abortifacients?

A

Drugs that induce abortion (not contraceptives)

423
Q

What do oral contraceptives do and their effects? (3)

A

Contain estrogen and progesterone that inhibit pituitary gonadotropins (prevent ovulation), thicken cervical mucous (decr sperm movements), inhibits proliferation of endometrium by estrogen (decr receptivity)

424
Q

What are 2 types of oral contraceptives?

A

Estrogen and progesterone (combination); progesterone only (mini-pill)

425
Q

What is a reason to take the mini-pill?

A

Lack of estrogen allows a nursing mother to lactate (estrogen inhibits PRL release)

426
Q

What do oral contraceptives mimic?

A

Luteal phase of menstrual cycle (keep est and prog steady, decr gonadotropins/LH surge)

427
Q

T/f: estrogen in oral contraceptives is high enough to exhibit +FB effects

A

False

428
Q

When is post-coital/emergency contraception taken?

A

Within 72 hours of intercourse

429
Q

What do emergency contraceptives interfere with? (3)

A

Ovulation, transport of conceptus to uterus (inhibit cilia in Fallopian tube), implantation (decr endometrial receptivity)

430
Q

What are 2 approaches to emergency contraceptives? Diff?

A

High dose est and prog: -FB inhibits ovulation

Mifepristone (RU486): progesterone antagonist (in uterus)

431
Q

How does Mifepristone (RU486) work? (2)

A

Binds to progesterone receptors in uterus (antagonist) causing: endometrium erosion and incr contractions of Fallopian tube and myometrium (incr prostaglandins) -abortifacient/contraceptive

432
Q

When is onset of menopause?

A

50-52 years old

433
Q

What is the initial stage of menopause called?

A

Perimenopause

434
Q

How is menopause onset detected?

A

With irregular menstrual cycles

435
Q

T/f: menopause is more abrupt than andropause

A

True, est decline&raquo_space; test decline

436
Q

When is menopause “declared”?

A

W/ cessation of menstrual cycles for 12 months

437
Q

Why are there psychological changes in menopause?

A

Accepting reproductive life has ended

438
Q

What is the cause of menopause? 3 effects?

A

Ovarian failure; decr responsiveness to gonadotropins, follicles lost to atresia, decr estrogen and inhibin decr -FB on HPG so incr GnRH and gonadotropins (no foll to respond to)

439
Q

T/f: the adrenal gland can still produce androgens after menopause

A

True

440
Q

Are adrenal androgens (converted to estrogen in tissues w/ aromatase) adequate to maintain estrogen-dependent tissues?

A

No, estrone (form prominent in post-menopausal women) is not sufficient to support estrogen-dependent tissues

441
Q

What are 5 physiological effects of decr estrogen activity in post-menopausal women?

A

Atrophy of breast and reproductive organs, osteoporosis, hot flashes (perimenopause), incr risk of CV disease, thinning and drying of vagina

442
Q

What is a possible treatment for menopause? Pro and con?

A

Hormone replacement therapy; pro: can manage symptoms during perimenopausal period, con: incr risk for CV disease

PHYSL 214 (6 decks)

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