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Physiology > BIOL 0800 Reading- Chapter 17 > Flashcards

BIOL 0800 Reading- Chapter 17 Flashcards

1
Q

What are the major sex hormones (gonadal steroids) in the male and female systems?

A

Testosterone, estradiol/progesterone

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2
Q

What hormone group does testosterone belong to?

A

Androgens: testosterone produced in testes, other less-potent androgens produced in adrenal cortex

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3
Q

What are the three major estrogens?

A

Estrone, estriol, and estradiol

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4
Q

Where are estrogens produced?

A

Ovaries and placenta

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5
Q

Which is the predominant estrogen?

A

Estradiol

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6
Q

How does estriol differ from estradiol and estrone?

A

Found only in pregnant women, produced only by placenta

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7
Q

How are all estrogens produced?

A

By aromatase from the precursor androgens

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8
Q

Where is progesterone produced?

A

Ovaries at specific times of menstrual cycle

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9
Q

How do all steroid hormones act?

A

Bind to intracellular receptors, which binds to nucleus DNA to alter mRNA function rate: changes protein synthesis rate

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10
Q

Which is the first hormone in the chain of controlling reproductive function?

A

GnRH: gonadotropin releasing hormone

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11
Q

Where does GnRH come from?

A

Hypothalamus; goes to anterior pituitary visual hypothalamo-pituitary portal blood vessels

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12
Q

What triggers secretion of GnRH?

A

Action potentials in GnRH-producing hypothalamic neuroendocrine cells: pulsatile pattern

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13
Q

Why is it important that action potential to neuroendocrine cells of the hypothalamus are pulsatile for secretion of GnRH?

A

Because the cells of the anterior pituitary that secrete gonadotropins become insensitive to GnRH in high concentrations

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14
Q

What two anterior pituitary hormones does GnRH stimulate?

A

Gonadotropins: FSH and LH

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15
Q

What do FSH and LH do in both sexes?

A

Stimulate maturation of sperm/ova; stimulate sex hormone secretion

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16
Q

What is the dual function of the gonads?

A

Gametogenesis and secretion of sex hormones

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17
Q

What is the first stage in gametogenesis?

A

Proliferation of primordial germ cells: mitosis, all have 46 chromosomes, ready to be split into gametes by meiosis

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18
Q

When does germ cell proliferation occur in males vs females?

A

Females: in fetal development; Males: in puberty and continues throughout life

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19
Q

What is the second stage of gametogenesis?

A

Meiosis: germ cells divide twice to produce haploid cells with 23 chromosomes each

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20
Q

What are Barr bodies?

A

When there are two X chromosomes, the nonfunctional one condenses into a nuclear mass: sex chromatin/Barr Body

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21
Q

What level of sex differentiation is controlled by the genes?

A

Only the presence of ovaries/testes: all other characteristics are controlled by presence/absence of proper hormones

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22
Q

What determines formation of testes rather than continued formation of ovaries?

A

SRY gene: codes for SRY protein that activates a sequence of events in the urogenital ridge; only found on Y chromosome

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23
Q

What are the two components of the primitive reproductive tract?

A

Mullerian ducts and Wolffian ducts

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24
Q

Which duct, Mullerian or Wolffian, persists in males vs females?

A

Wolffian for male, Mullerian for female

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25
Q

What is MIS?

A

Mullerian-inhibiting substance: secreted by the testes along with testosterone; gene is encoded on the SRY gene of the Y chromosome

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26
Q

The testes secrete testosterone and MIS to begin male sex differentiation. What does testosterone do to help differentiation?

A

Stimulates differentiation of Wolffian ducts into epididymis, vas deferens, ejaculatory duct, and seminal vesicles

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27
Q

What hormones stimulates differentiation of Wolffian ducts into epididymis, vas deferens, seminal vesicles, and ejaculatory duct?

A

Testosterone

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28
Q

What is DHT?

A

Hormone produced from testosterone: stimulates formation of a penis and scrotum

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29
Q

What hormone causes the testes to descend into the scrotum?

A

Testosterone

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30
Q

What is cryptorchidism?

A

Failure of the testes to descend into the scrotum

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31
Q

What happens in Y-less, SRY-less, MIS-less females?

A

Mullerian ducts develop into fallopian tubes and uterus; Wolffian ducts degenerate without testosterone, and vagina/external genitalia develop

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32
Q

What is androgen insensitivity syndrome?

A

Genotype is XY, testes are present but androgen-receptor gene is mutated: testes secrete MIS and testosterone, so Mullerian ducts degenerate, but Wolffian ducts can’t respond to testosterone, so they also degenerate and vagina/external genitalia develop as in females

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33
Q

What is congenital adrenal hyperplasia?

A

Production of too much androgen in fetus, due to mutation in gene for enzyme in cortisol synthetic pathway: decrease in cortisol, increased ACTH, increased androgen production; results in masculinized XX fetus

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34
Q

What are sexual dimorphisms?

A

Sex-linked differences in appearance or form within a species

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35
Q

What are Leydig cells?

A

Interstitial cells that lie in small connective-tissue spaces between seminiferous tubules in the tests: synthesize and release testosterone

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36
Q

What male reproductive structure produces sperm?

A

Seminiferous tubules

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37
Q

What male reproductive structure produces testosterone?

A

Leydig cells

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38
Q

What is the rete testis?

A

The network of interconnected tubes formed when the seminiferous tubules converge

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39
Q

What is the epididymis?

A

The structure attached to the outside of the testis; carries efferent ductules from the rete testis to the vas deferens

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40
Q

What is the vas deferens?

A

Large, thick-walled tubule lined with smooth muscle: bound with vessels/nerves in the spermatic cord (which passes to the testis through the inguinal canal from the abdominal wall)

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41
Q

What are the seminal vesicles?

A

Two large glands behind bladder that join the two vas deferens to form the two ejaculatory ducts

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42
Q

What happens after the seminal vesicles join the vas deferens to form the ejaculatory ducts?

A

Ejaculatory ducts enter the prostate gland and join the urethra, coming from the bladder

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43
Q

What is the prostate gland?

A

Doughnut shaped: surrounds upper part of urethra to secrete fluid into it

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44
Q

What are the bulbourethral glands?

A

Lie below the prostate: drain into the urethra as it leaves the prostate

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45
Q

Which male reproductive structures secrete semen?

A

Prostate gland and seminal vesicles

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46
Q

What do the bulbourethral glands contribute to semen?

A

Small amounts of lubricating mucoid secretions

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47
Q

What are spermatogonia?

A

Undifferentiated germ cells

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48
Q

What are primary spermatocytes?

A

The cells that result from the final mitotic division and differentiation in the series of spermatogonium proliferation

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49
Q

How does the male reproductive system maintain spermatogonia supply if the spermatogonia are converted into primary spermatocytes?

A

Not all of them do: one of the cells of each clone drops out of the mitosis-differentiation cycle to remain as a stem cell spermatogonium

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50
Q

What are secondary spermatocytes?

A

Cells formed from the first meiotic division of primary spermatocytes: contain 23 two-chromatid chromosomes

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51
Q

What are spermatids?

A

Cells formed from the second meiotic division of primary spermatocytes, or the division of the secondary spermatocytes: contained 23 one-chromatid chromosomes

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52
Q

What is the final phase of spermatogenesis?

A

Differentiation of spermatids into spermatozoa

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53
Q

What is the acrosome?

A

A protein filled vesicle with several enzymes needed for fertilization

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54
Q

What are Sertoli cells?

A

Cells that extend from the basement membrane of the seminiferous tubules to the lumen; joined to adjacent Sertoli cells by tight junction; form an unbroken ring around the outer circumference of seminiferous tubule: tight junctions divide the tubule into two compartments: basal compartment and central compartments

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55
Q

What are the two compartments of the seminiferous tubule lumen?

A

Basal compartment (between basement membrane and tight junctions) and central compartment (between tight junctions and including the lumen)

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56
Q

What is the Sertoli cell barrier?

A

The blood-testes barrier: prevents movement of chemicals into seminiferous tubule lumen

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57
Q

Where does mitotic cell division/differentiation of spermatogonia occur?

A

Basal compartment of the seminiferous tubule

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58
Q

Where do meiotic divisions of primary spermatocytes occur?

A

Central compartment of the seminiferous tubule

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59
Q

What do the Sertoli cells do in the seminiferous tubules?

A

Serve as route for nutrients for developing germ cells, secrete most of fluid in seminiferous tubule lumen

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60
Q

What is ABP?

A

Androgen-binding protein: binds testosterone secreted by Leydig cells so it can cross the Sertoli cell barrier to enter the seminiferous tubule

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61
Q

What is the pathway for sperm after production in the central compartment of the seminiferous tubules?

A

Through the rete testis to the efferent ductules to the epididymis to the vas deferens for storage in the vas deferens/epididymis

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62
Q

What generates sperm movement as far as the epididymis?

A

Secretion of fluid by the Sertoli cells; creates pressure and moves the sperm/fluid

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63
Q

What generates sperm movement through the epididymis?

A

Peristaltic contractions of smooth muscle in epididymis and vas deferens: sperm are gathered in tight mass, since fluid was reabsorbed from the epididymal lumen

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64
Q

What neural input is needed for erection?

A

Inhibition of sympathetic input; activation of nonadrenergic, noncholinergic autonomic neurons to arteries: release nitric oxide to release arterial smooth muscle and allow vasodilation

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65
Q

What kinds of neurons release NO to the arteries of the penis to allow vasodilation for erection?

A

Nonadrenergic, noncholinergis autonomic neurons

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66
Q

How does NO cause vasodilation for erection?

A

Stimulates guanylyl cyclase, to catalyze formation of cGMP, which triggers a signal transduction pathway to relax arterial smooth muscle

67
Q

What kind of reflex is ejaculation?

A

A spinal reflex mediated by afferent pathways from penile mechanoreceptors

68
Q

What are the two phases of ejaculation?

A

Smooth muscle phase (epididymis, vas deferens, ejaculatory ducts, prostate, and seminal vesicles contract as a result of sympathetic nerve stimulation, to empty sperm and glandular secretions into urethra), Semen phase (semen expelled from urethra by rapid contractions of urethral smooth muscle and skeletal muscle at base of penis)

69
Q

What is the difference between FSH and LH’s action in the testes?

A

FSH affects Sertoli cells (stimulates secretion of paracrine agents required for spermatogenesis); LH affects Leydig cells (stimulates testosterone secretion)

70
Q

FSH and LH affect which kind of cells, each?

A

FSH affects Sertoli, LH affects Leydig; FS(ertoli)H, L(eydig)H

71
Q

How does LH have an indirect effect on spermatogenesis if FSH-induced Sertoli action is central to spermatogenesis?

A

The testosterone produced by Leydig cells under influence of LH is crucial to spermatogenesis

72
Q

What are the two ways testosterone inhibits LH secretion through negative feedback?

A

Acts on hypothalamus to decreased GnRH burst amplitude (decrease in gonadotropin secretion); Acts on anterior pituitary to decrease LH response to a given amount of GnRH

73
Q

How is FSH secretion inhibited through negative feedback from the testes?

A

Sertoli cells in the testes secrete inhibin, which acts on the anterior pituitary gland to reduce secretion of FSH; negative feedback because FSH stimulates Sertoli cell paracrine agents, spermatogenesis, and inhibin production

74
Q

How is testosterone converted into DHT in the prostate?

A

By enzyme 5-alpha-reductase

75
Q

What happens to testosterone in the brain?

A

Converted into estradiol by aromatase

76
Q

What causes the first early signs of puberty in males?

A

Increased secretion of adrenal androgens, probably under stimulation of adrenocorticotropic hormone (ACTH)

77
Q

Why do men have a higher hematocrit than women?

A

Because androgens stimulated during puberty stimulate secretion of erythropoietin

78
Q

What is Klinefelter’s Syndrome?

A

Genetic hypogonadism: most commonly caused by XXY: meiotic nondisjunction; abnormal Leydig function, lack of testosterone to decrease secondary sex characteristics

79
Q

What is secondary hypogonadism?

A

Hypogonadism caused by decreased LH/FSH secretion; most commonly caused by hyperprolactinemia, since prolactin inhibits FSH/LH

80
Q

What is meiotic arrest?

A

The condition in females that all eggs present at birth are primary oocytes, converted from oogonia; meiotic division into secondary oocytes does not complete yet, but replication of DNA does

81
Q

When does the first meiotic division occur in oogenesis?

A

After meiotic arrest, right before ovulation

82
Q

What happens during the second meiotic division, during formation of the secondary oocyte?

A

One of the daughter cells retains the cytoplasm, the other remains small and nonfunctional as a polar body

83
Q

Where does the second meiotic division occur in oogenesis?

A

In the fallopian tube AFTER ovulation, IFF the secondary oocyte is fertilized

84
Q

What is the primary follicle?

A

The primary oocyte plus a layer of granulosa cells

85
Q

What happens during development from the primordial follicle stage?

A

Increase in oocyte stage, proliferation of granulosa cells into multiple layers, separation of oocyte from inner granulosa by a thicker layer of zona pellucida

86
Q

What is the zona pellucida?

A

Contains glycoproteins to help bind sperm cell to egg surface

87
Q

What do granulosa cells do?

A

Secrete estrogen, small amounts of progesterone before ovulation, and inhibiin

88
Q

How do inner granulosa cells communicate with the oocyte despite the zona pellucida?

A

Through gap junctions between the zona pellucida and the oocyte

89
Q

What happens as the follicle grows by mitosis of granulosa cells, after development of the zona pellucida?

A

Development of the theca by differentiation of granulosa cells

90
Q

What is the theca?

A

Differentiated outer layers of granulosa cells; important role in estrogen secretion by granulosa cells

91
Q

What happens after theca development?

A

Primary oocyte reaches full size, antrum develops between granulosa cells and the zona pellucida around the oocyte

92
Q

What is the antrum?

A

The fluid surrounding the primary oocyte encased in zona pellucida and granulosa cells; fluid produced by granulosa cells

93
Q

What is atresia?

A

Degeneration of non-dominant follicles; the primary oocytes encased also die

94
Q

When does atresia occur?

A

At any time: the follicle does not have to be antral; continues throughout life

95
Q

What happens to granulosa cells as the dominant follicle begins to expand?

A

The granulosa cells around the egg form a mount that projects into the antrum: cumulus oophorous

96
Q

What is the cumulus oophorous?

A

The mound of granulosa cells and primary oocyte that extends into the antrum during dominant follicle enlargement

97
Q

What happens to the dominant follicle around ovulation?

A

The primary oocyte leaves meiotic arrest, finished the first meiotic division to become a secondary oocyte; cumulus oophorous separates from the follicle wall, floats in antral fluid; the mature follicle balloons out from ovary surface

98
Q

What occurs during ovulation?

A

The thin walls of the follicle and ovary rupture because of enzymatic digestion; secondary oocyte with zona pellucida/granulosa/cumulus carried out of ovary onto ovarian surface by antral fluid

99
Q

What happens to the follicle after ovulation?

A

Degenerates into corpus luteum: granulosa cells enlarge, becomes glandlike; secretes estrogen, progesterone, and inhibin

100
Q

Where does estrogen come from during the menstrual cycle?

A

Synthesized/released from granulosa cells in follicular phase; synthesized/released from corpus luteum in luteal phase

101
Q

Where does progesterone come form during the menstrual cycle?

A

Synthesized/released in SMALL amounts in granulosa/theca; major source: corpus luteum during luteal phase

102
Q

Where does inhibin come from during the menstrual cycle?

A

Secreted by granulosa cells and corpus luteum

103
Q

What trend does FSH show across the menstrual cycle?

A

Increases in early follicular phase, then decreases throughout rest of cycle; EXCEPT: small peak around ovulation; small increase while transitioning from one cycle to the next

104
Q

What trend does LH show across the menstrual cycle?

A

Stead throughout cycle EXCEPT for huge surge around ovulation; constant decline throughout luteal phase

105
Q

What trend does estrogen show across the menstrual cycle?

A

Increases during second week as dominant follicle grows; decreases shortly before LH surge; increases again after formation of corpus luteum; rapid decrease in late luteal phase

106
Q

What trend does progesterone show across the menstrual cycle?

A

Low concentrations until formation of corpus luteum

107
Q

What trend does inhibin show across the menstrual cycle?

A

Similar to estrogen: large peak between second week and right before LH surge, second peak after formation of corpus luteum, decrease in late luteal phase

108
Q

Why is there a small increase in FSH to transition from one menstrual cycle to the next?

A

FSH required for stimulation of follicle development: caused by decreased progesterone, estrogen, and inhibin

109
Q

What causes the small increase in FSH at the end of the menstrual cycle?

A

Decrease in estrogen, progesterone, and inhibin from degeneration of the corpus luteum: removal of negative feedback

110
Q

Which types of cells, granulosa or theca, do FSH and LH act on?

A

FSH on granulosa, LH on theca (fish granola, in the lake-a)

111
Q

What two hormones stimulate proliferation of granulosa cells in the early follicular phase?

A

FSH and estrogen: FSH stimulates granulosa cells to multiply and product estrogen; estrogen acts as paracrine agent for more granulosa cells

112
Q

How do theca cells help granulosa cells produce estrogen?

A

By providing the androgen precursors needed to make estrogen: LH acts on theca cells to produce androgens, which are converted in granulosa cells by aromatase into estrogen

113
Q

How does LH indirectly influence granulosa cells estrogen-secretion?

A

LH stimulates theca cells, which produce androgens to be converted in the granulosa cells into estrogen

114
Q

How are granulosa/theca similar to Sertoli/Leydig?

A

Sertoli/granulosa control germ development environment and are stimulated by FSH and the major gonadal sex hormone (estrogen vs testosterone); Leydig/theca produce androgens and are stimulated by LH

115
Q

Why do nondominant follicles degenerate?

A

Because of the decrease in FSH during the second week: necessary for follicular development

116
Q

Why can the dominant follicle survive even during the decreased FSH levels?

A

Because they have increased sensitivity to FSH, and the increased number of granulosa cells are also stimulated by LH, which is stable/starting to surge

117
Q

Why is there a drop in FSH around the second week of the cycle?

A

Because as the dominant follicle develops LH receptors, more estrogen is produced: estrogen acts as negative feedback for FSH and LH by the anterior pituitary

118
Q

Why does FSH decrease more than LH in the presence of increased estrogen?

A

Because the granulosa cells also secrete inhibin, which acts more on FSH than LH, if at all

119
Q

How does the feedback effect of estrogen vary from low to high concentrations of estrogen?

A

Low concentrations are inhibitory to FSH/LH, but high concentrations are stimulatory: causes LH surge

120
Q

What causes the LH surge?

A

Positive feedback by high levels of estrogen caused by increased granulosa proliferation and estrogen secretion, from the previous FSH levels

121
Q

Where do the LH-induced ovulation-causing actions occur?

A

In the granulosa cells

122
Q

What are the two main functions of the LH surge?

A

Induce ovulation; transform the leftover follicle into corpus luteum

123
Q

What three substances does the corpus luteum primarily produce?

A

Progesterone, estrogen, and inhibin

124
Q

Why are gonadotropin concentrations low in the luteal phase?

A

High progesterone inhibits the anterior pituitary secretion of FSH/LH and suppresses GnRH from the hypothalamus; inhibin also inhibits FSH secretion

125
Q

How do ovarian phases match up with uterine phases?

A

Follicular phase (menstrual and proliferative), vs luteal (secretory)

126
Q

What causes/occurs during the proliferative phase?

A

Increased levels of estrogen: causes endometrium growth and myometrium growth; induces progesterone receptor synthesis

127
Q

What is the myometrium?

A

The layer of uterine smooth muscle under the endometrium

128
Q

What happens to the endometrium after ovulation?

A

Progesterone acts on newly-formed receptors to convert the endometrium into a secretory tissues: secretes glycogen, glycoproteins, and mucopolysaccharides; progesterone inhibits myometrial contractions

129
Q

What is the first (and second) event causing menstruation, after the decrease in progesterone/estrogen from the corpus luteum degeneration?

A

Vasoconstriction of the endometrium: then uterine contractions

130
Q

What causes myometrial contractions in menstruation?

A

Prostaglandins

131
Q

What causes menstrual bleeding?

A

Endometrial vasodilation (after the severe vasoconstriction), which results in hemorrhage through the weakened capillary walls

132
Q

What causes menopause?

A

Ovarian failure: ovaries can’t response to gonadotropins; follicles and eggs degenerated through atresia

133
Q

How does the egg get from the ovary to the fallopian tubes?

A

The fimbriae’s cilia bring it in after it’s been extruded from the ovary onto the surface

134
Q

What is capacitation?

A

The process by which sperm are acted upon by vaginal tract secretions to enable fertilization

135
Q

What are the two effects of capacitation?

A

Change in sperm flagellum movement from wavelike to whiplike, and alteration of sperm membrane to be capable of fusing with the egg membrane

136
Q

What happens during fertilization?

A

The sperm moves between granulosa cells of the zona pellucida; binds to glycoproteins, triggering the acrosomal reaction

137
Q

What is the acrosomal reaction?

A

When the plasma membrane of the sperm head is altered so that the underlying membrane0bound acrosomal enzymes are not exposed to the zona pellucida: digests a path to the egg membrane

138
Q

How does block to polyspermy occur?

A

The binding changes the membrane potential; the cortical reaction: cytosolic secretory vesicles release contents into extracellular space between egg and zona pellucida; harden the zona pellucida and inactivate the sperm-binding sites

139
Q

Why does the conceptus stay in the fallopian tubes for a few days after fertilization?

A

Because the high levels of estrogen keep the smooth muscle contracted near where the tube enters the uterus; then increased progesterone allows it to relax

140
Q

What does it mean that the 16- to 32-cell conceptus is totipotent?

A

That each cell in the conceptus is capable of becoming an individual: how identical twins develop

141
Q

What is a blastocyst?

A

The next stage of the conceptus after zygote to morula; cells begin to differentiate and no more totipotentiality

142
Q

What are the three components of the blastocyst?

A

Trophoblast (outer layer), inner cell mass, and central fluid-filled cavity

143
Q

What happens when the blastocyst implants into the endometrium?

A

Trophoblast proliferates rapidly to penetrate the endometrium; blastocyst buries itself with the help of proteolytic enzymes; allows endometrium to deliver nutrients to the embryo

144
Q

What structure takes over for the endometrium to provide nutrients for the embryo?

A

Placenta: interlocking fetal and maternal tissues that serves as an exchange between the mother and fetus

145
Q

What is the chorion?

A

The embryonic part of the placenta; outer layer of trophoblast cells; extends as chorionic villi into the endometrium

146
Q

How does maternal blood enter the placental sinuses to reach the chorionic villi of the placenta?

A

Through the uterine artery; exits through the uterine veins

147
Q

Describe the structure of the umbilical cord.

A

Fetal blood leaves capillaries of chorionic villi to go to umbilical arteries; blood comes back to fetus through umbilical veins from the chorionic villi

148
Q

What is the amniotic cavity?

A

A space between the inner cell mass and the chorion; lined by the amniotic sac, which eventually fuses with the chorion to provide one lining for the fetus

149
Q

What happens to estrogen and progesterone levels during pregnancy?

A

Get higher and higher!!

150
Q

Why doesn’t the corpus luteum dissolve throughout pregnancy?

A

Because it’s maintained by hCG, secreted by the trophoblast cells

151
Q

What does hCG do?

A

Prevents dissolution of the corpus luteum; stimulates steroid secretion

152
Q

What happens when hCG levels drop back down?

A

Placenta begins to secrete large quantities of estrogen and progesterone; originally from corpus luteum, but then from the trophoblast cells

153
Q

What does human placental lactogen do?

A

Mobilizes fats from maternal adipose tissue; stimulates glucose production in the liver; stimulates breast development for lactation

154
Q

What happens to the smooth muscle cells of the myometrium once parturition begins?

A

Synthesize connexins to form gap junctions, allowing the myometrium to coordinate contractions

155
Q

How does the cervix become soft at the beginning of parturition?

A

Estrogen, which also stimulated prostaglandins; also relaxin from the ovaries

156
Q

What are the two main functions of oxytocin during birth?

A

Potent uterine muscle stimulant; also stimulates secretion of prostaglandins to help stimulate uterine smooth muscle contraction further

157
Q

What do prostaglandins to do the late antral follicle?

A

Stimulate production of digestive enzymes to rupture the follicle

158
Q

What do prostaglandins to do the corpus luteum?

A

Interfere with hormone secretion and function; cause death of the corpus luteum

159
Q

What do prostaglandins to do the uterus?

A

Constrict endometrial blood vessels to begin menstruation; cause changes in endometrial vessels/cells in early pregnancy to facilitate implantation; increase myometrial contraction to initiate menstruation and parturition; cause cervical ripening to allow dilation

160
Q

Which two hormones inhibit/stimulate secretion of prolactin from the anterior pituitary?

A

Dopamine inhibits, prolactin-releasing factor stimulates

161
Q

Why is there no lactation throughout pregnancy?

A

Because action of prolactin on the breasts is inhibited by the large concentration of estrogen and progesterone

162
Q

What allows milk ejection reflex?

A

Oxytocin: reflexively released from posterior pituitary in response to suckling

163
Q

What s the milk ejection reflex?

A

When milk produced by the alveoli is pushed into the ducts by contraction of the myoepithelial cells

Physiology (13 decks)

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