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Physiology > Reproductive Physio > Flashcards

Reproductive Physio Flashcards

1
Q

what happens first in female pubertal development?

A

thelarche- breast budding (coincides with increase in estrogen)
then adrenarche - pubic hair

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2
Q

when does menarche occur?

A

first menses- between 11-14, average 12.5 (later than 2.5 years after beast development is abnormal)

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3
Q

when is puberty considered precocious? what is a concern?

A

6 for girls, 9 for boys

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4
Q

when does no pubertal development warrant investigation?

A

13 years old and no breast development

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5
Q

What difference in tanner stages between tissues is abnormal?

A

> 2

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6
Q

What is the first sign of male pubertal development

A

increase in testicular volume >3 ml (increased FSH); tanner stage 2

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7
Q

Normal menstrual cycles depend on _____ feedback provided by estrogen to the hypothalamus and pituitary

A

positive

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8
Q

important tanner stages for breasts

A

3- adult but smaller

4- nipple froms secondary mound

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9
Q

during what tanner stage does pubic hair become coarse and curly and extend to pubis?

A

tanner 3

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10
Q

lab evaluations for precocious puberty

A
  • bone scan (looking for advanced skeletal maturation)
  • brain MRI
  • labs w/ and w/o stimulation (FSH/LH/testosterone/DHEA)
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11
Q

when does menarche occur?

A

first menses- between 11-14, average 12.5 (later than 2.5 years after beast development is abnormal)

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12
Q

pathway of sexual differentiation

A 
genetic sex (chromosomes) 
gonadal sex (testes/ovaries) 
genital sex (external genitalia)
gender sex (behavior)
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13
Q

what is required for testicular development?

A

SRY on Y chromosome

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14
Q

what is required for ovary development?

A

two X chromosomes (still get female ducts & genitalia b/c default pathway is female, don’t have Y, progression to female structures occurs when male hormones are absent)

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15
Q

when does the female germ cell arrest?

A

during meiosis 1, substage of prophase

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16
Q

what is the product of male vs female meiosis?

A

Male- 4 daughter cells/germ cell (spermatogenesis)

Female- 1 daughter cell/germ cell + polar body

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17
Q

what does normal sperm development require?

A

reduced body temperature

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18
Q

what are some defects in genetic sex?

A
  • aneuploidy- # chromosomes
  • mosaicism- different genotypes in different cells
  • chimerism - fused zygotes
  • structural errors- unequal recombination
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19
Q

T/F Sexual dimorphism of phenotypic sex due to male vs female hormones/receptors

A

False- due to differences in the amounts of hormones and patterns of secretion

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20
Q

what happens if, while genital ducts are maturing they encounter testosterone? antimullerian hormone?
what produces each?

A

w/ testosterone from leydig cells (normally from testes), keep wolffian ducts

w/ antimullerian hormone from sertoli cells- degrade mullarian ducts

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21
Q

what happens if, while genital ducts are maturing they encounter no testosterone or antimullerian hormone? (aka have no testes)

A

no testosterone- wolffian ducts regress

no AMH- keep mullarian ducts, develop fallopian tube, cervix, upper vagina

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22
Q

what does 5 alpha reductase do?

A

converts testosterone to more potent DHT, which is important for male genitalia development via androgen receptors

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23
Q

what does finesteride (propecia) block?

A

5 alpha reductase; DHT has mitogenic effect on prostate gland, can cause benign prostatic hypertrophy
BUT
if encountered by fetus, can prevent male external genitalia development

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24
Q

differentiation of external genitalia?

A
  • genital tubercle- citorus/glans penis
  • urogenital folds- labia minora/ventral penis
  • labioscrotal folds- labia majora/scrotum
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25
Q

male psudohermaphroditism and example

A

if testes + some/all female tract, female external genitalia
e.g. androgen resistance - no public hair, undescended testes

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26
Q

what is turner’s syndrome?

A

2nd x chromosome is inactivated, get streak gonads instead of ovaries

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27
Q

female pseudohermaphroditism

A

if ovaries + some/all of male tract+ male external genitalia

e. g. adrenal hyperplasia/virilizing ovarian tumor in mom
- clitoral hypertrophy, get fusion of urogenital sinus
- androgens lead to advanced skeletal age

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28
Q

describe kleinfelter’s syndrome

A

XXY - phenotypic male w/ no seminiferous tubule development, low testosterone, long legs, flat topped pubic hair

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29
Q

where does spermatogenesis occur?

A

seminiferous tubules

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30
Q

what do germ cells become?

A

spermatogonia in male, oogonia in female

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31
Q

what do coelomic epithelium cells become?

A

sertoli cells in male, granulosa cells in female (nurse cells)

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32
Q

what do mesenchymal cells become?

A

leydig cells in males, theca cells in females (hormone cells)

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33
Q

what converts testosterone to estadiol?

A

aromatase

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34
Q

what converts testosterone to DHT?

A

5 alpha reductase

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35
Q

what does testosterone do during fetal development?

A

epididymis
vas deferens
seminal vesicles

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36
Q

what does DHT do during fetal development?

A

penis/urethera
scrotum
prostate

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37
Q

what does testosterone do during puberty?

A 
penis
seminal vesicles
musculature
voice
skeleton
spermatogenesis
38
Q

what does DHT do during puberty?

A 
scrotum
prostate
male pattern baldness
happy trail
beards
sebaceous glands
39
Q

T/F Hormones come from the testes and seminal vesicles

A

FALSE- only from the testes

40
Q

spermatogenesis

A

process of sperm production

41
Q

spermiogenesis

A

cellular remodeling of spermatids into spermatazoa

  • get nuclear condensation
  • shrink the cytoplasm
  • form the acrosome
  • develop the tail
42
Q

spermeation

A

extrusion of flagellated spermatozoa into the lumen of the tubule
- residual body is formed

43
Q

what are intracellular bridges?

A

connect secondary spermatocytes to sertoli cells; synchronizes development of a group of cells, allows sharing of resources

44
Q

what does the first meiotic division produce in men? the second?

A

first- secondary spermatocytes with 23 chromosome pairs

second- spermatids with 23 single chromosomes

45
Q

what is the acrosome?

A

a cap of membranes containing digestive enzymes

46
Q

function of the epididymis

A
  • sperm maturation (gain motility, lose cytoplasm)
  • reservoir for sperm
  • stabilize acrosome
47
Q

function of prostate

A
  • secrete alkaline fluids to neutralize vagina

- makes PSA (prostate specific antigen)

48
Q

function of seminal vesicle

A
  • secrete prostaglandins which stimulate uterus & fallopian tube contraction
49
Q

describe the male neuroendocrine axis

A

hypothalamus (arcuate and POA)- GnRH
pituitary (gonadotrophs)- FSH/LH
gonads- testosterone in men, estradiol in women

50
Q

what kind of feedback do the gonads provide?

A 
negative on hypothalamus/pituitary
* testosterone/estradiol
* follistatin
* inhibin 
positive on pituitary
* activin
51
Q

what stimulates the hypothalamus in the gonad endocrine pathway?

A

stimulated by: NE (norepinephrine)

inhibited by: dopamine/endorphins

52
Q

what are leydig cells stimulated by and what do they do?

A
  • stimulated by LH to secrete testosterone
  • GPCR/PKA mechanism to increase transcription
  • also increases expression of carrier protein & activating protein
  • stimulated indirectly by FSH-inhibin
53
Q

what are sertoli cells stimulated by and what do they do?

A
  • stimulated by androgens and FSH to facilitate sperm development
  • GPCR/PKA mechanism to increase transcription
  • also increases androgen binding protein/androgen receptors
  • activates aromatase, converting testosterone to estradiol
  • increases growth factors
  • increases inhibin, AMH
54
Q

what is the paracrine function of inhibin?

A

stimulates testosterone secretion (activin inhibits testosterone secretion)

55
Q

what happens if spermatogenesis is too fast?

A

germ cells stimulate sertoli cells to increase inhibin (acts on hypothalamus/pituitary)- decreases spermatogenesis

56
Q

erection is under ___ control releasing __ and __ which produces ___, leading to vasodilation

A

parasympathetic, Ach, NO, cGMP

57
Q

emission is under ___ control

A

sympathetic; direct innervation by alpha adrenergic receptors

58
Q

ejaculation is under ____ control

A

spinal reflex:

  • entry of semen
  • afferents reach S2-S4
  • trigger pudendal nerve
  • get rhythmic contractions of ischio and bulbo muscles
59
Q

what is primary hypogonadism?

A
  • hypergonadotropic hypogonadism
  • high LH/FSH, decreased testosterone/DHT
    includes
  • defective antrogen synthesis
  • kleinfelters (XXY)
  • hermaphroditism
60
Q

what is secondary/tertiary hypogonadism?

A
  • hypogonadotrophic hypogonadism
  • decreased LH/FSH, decreased testosterone/DHT
    includes
  • Kallmann’s syndrome
  • hyperprolactinemia
  • anorexia
  • estrogen supression of LH
61
Q

what does the follicle consist of?

A
  • one oocyte surrounded by a cluster of granulosa cells
62
Q

stages of follicular development

A
  • primordial follicle- inactive, 90-95%
  • primary follicle- gains granulosa cells, oocyte grows
  • secondary follicle - a couple induced by FSH, antrum forms
  • graafian (mature) follicle - antrum enlarges, one is dominant, exponential growth
63
Q

events of ovulation

A
  • follicle ruptures, proteolysis of basement membrane, oocyte in peritoneal cavity
  • fimbriae draw oocyte in
  • meiotic division is completed
  • other follicles die
  • corpus luteum is formed
64
Q

what does the corpus luteum secrete?

A

progesterone (moderate levels of estradiol and inhibin A)

65
Q

how is inhibin involved in the female pathway? two types?

A
  • produced by granulosa cells of follicle following stimulation by FSH
  • inhibin inhibits FSH release by gonadotrophs
    inhibin B- dominant follicle
    inhibin A- corpus luteum
  • lull between the two at ovulation
66
Q

dominant estrogen in ovary

A

estradiol (E2) - from cholesterol, aromatase is necessary, transported via SHBG

67
Q

where does GnRH come from? what is it inhibited/stimulated by?

A
  • arcuate nucleus and preoptic area of hypothalamus;
  • inhibitors: dopamine, endorphins, CRH
    stimulator: NE
68
Q

what type of neurons is oxytocin secreted by?

A

magnocellular

69
Q

describe GnRH’s actions in pituitary

A
  • cuts phospholipase into IP3 and DAG
    1) IP3 releases Ca2+ from ER, causes exocytosis of FSH/LH vesicles
    2) DAG activates PKC which increases the synthesis of FSH/LH
70
Q

T/F Have distinct gonadotrophs for FSH and LH

A

FALSE

71
Q

what does FSH do?

A

stimulate follicular development

estradiol secretion

72
Q

what does LH do?

A

promotes ovulation and leutinization

73
Q

What inhibits activin?

A

follistatin

74
Q

what hormones do you find in the ovaries?

A
  • estrogens
  • progesterone
  • androgens (testosterone, DHT, DHEA)
  • inhibins and activins and follistatin
75
Q

3 menstrual phases

A

follicular (cycle length differences), ovulatory (1-3 days), luteal (14 days)

76
Q

hormone actions during follicular phase

A

1) GnRH causing FSH/LH release (pulsatile)
2) increasing FSH/LH stimulate ovary to develop follicle
3) follicle secretes E2 (estradiole)
4) E2 has positive feedback on follicle BUT
5) E2 has negative feedback (with inhibin) on pituitary/hypothalamus on FSH cells - keeps volume down as capacity builds (LH rising)

77
Q

hormone actions during ovulatory phase

A

1) E2 gets past a certain threshold for a sustained period of time, switches to positive feedback (timing determined by ovary)
1b) increase GnRH receptors on gonadotrophs
2) get LH surge - reinforcing self and E2
3) causes rupture of follicle
4) everything dips because it’s all disorganized

78
Q

hormone actions during luteal phase

A

1) corpus luteum becomes dominant- makes E2 (not as high as surge) and progesterone (off the charts)
2) switch back to inhibition, get little LH/FSH/GnRH
3) no LH causes corpus luteum to degrade
4) once CL degrades, lose E2 and progesterone, FSH levels recover
5) lose functional endometrial layer

79
Q

which hormone prevents the corpus luteum from degrading?

A

HCG

80
Q

what happens to androgens during the menstrual cycle?

A

testosterone bumps at the end of the follicular phase, increasing libido during ovulation

81
Q

modes of gonadotropin release in males vs females

A

males- tonic mode- low, pulsatile LH release

females- surge mode- periodic, massive LH release

82
Q

what are the relative ratios of LH:FSH throughout life?

A

FSH>LH during childhood
LH>FSH during reproductive period
FSH>LH in menopause (and in old males)

83
Q

What does a lack of LH/FSH receptors or lack of estrogen cause?

A

primordial follicles without primary follicles

84
Q

what are the actions of estradiol secreted by the dominant follicle?

A
  • inhibits growth of other follicles
  • makes mucus thin
  • prepares fallopian tubes
  • potentiates action of progesterone so uterus goes into secretory mode
  • primes GnRH action on LH surge to get more LH
85
Q

what is the 2 compartment theory?

A

theca cells take up cholesterol, make androstenedione, release it to granulosa cells, which have aromatase to convert testosterone to estradiol

86
Q

how does the corpus luteum start to form during follicular phase?

A
  • increase LH receptors on theca cells due to FSH actions
  • LH converts granulosa and theca–> lutein cells
  • lutein cells make lots of progesterone and estradiol
87
Q

phases in terms of endometrial functions?

A

proliferative, secretory, ischemic

88
Q

what hormone dominates in proliferative phase?

A

estradiol

89
Q

what hormone dominates the secretory phase?

A

progesterone - shift to secreting glycogen, mucus, increasing vascularization

90
Q

what changes the viscosity of cervical mucus?

A

estrogen’s actions in follicular phase

91
Q

what happens during menopause?

A
  • loss of negative feedback from estradiol
  • cause massive increase in FSH/LH
  • still have pulsatile secretion but no cyclicity
    causes:
    osteoporosis, CV disease, decreased breast mass, vascular flushing
92
Q

risks/benefits of hormone replacement therapy

A
  • when given late, can increase CHD, stroke, breast cancer (but decreases bone breaks)
  • when given early, might be beneficial

Physiology (22 decks)

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