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BIOL 2410 > Reproduction > Flashcards

Reproduction Flashcards

1
Q

male reproductive organs/gonad

A

testes

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2
Q

female reproductive organ/gonad

A

ovaries

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3
Q

gametogenesis

A

process by which sperm or ova are produced

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4
Q

gametes have an endocrine role, what are the ones involved in males and females?

A

males: testosterone

estrogens and progesterones in females

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5
Q

what is the role of reproductive tracts

A

house and transport gametes

males: vasdeferens
females: fallopian tubes

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6
Q

accessory sex glands

A

male: seminal vesicles, prostate, bulbourethral (cowper’s) glands,
female: bartholin’s glands, clitoris, breasts

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7
Q

where is sperm made

A

within the testes

-seminiferous tubules

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8
Q

testes development

A
  • testes develop from the gonadal ridge during development

- descend through the inguinal canal usually complete before 7 months gestation

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9
Q

what is cryptorchidism

A

when the testes don’t descend, staying up in the abdomen (one or both)
-this can lead to infertility

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10
Q

why do testes lie on the external side of the body?

A

testes are approx. 3 degrees lower than the rest of the body

  • this cooler temperature allows for better development of sperm (in humans)
  • other mammalian species are different
  • this temperature leads to improved mitochondrial development and better proliferation
  • better chance to fertilization
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11
Q

seminiferous tubule structure

A
  • immature spermatogonium on the outside, as you get closer to the inside, more mature sperm
  • leydig cells sit on the outiside and sertoli cells sit on the inside
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12
Q

____ cells lie within the basal lamina of the seminiferous tubules and release endocrine messages that direct development of spermatogonium into mature sperm

A

myoid

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13
Q

what is the role of the basal lamina in the seminiferous tubules of the testes?

A

acts like a blood brain barrier (with tight junctions) that serves as a defense mechanism for preventing messages that shouldn’t be there
-particularly stops the immune system from getting there and destroying chances for reproduction

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14
Q

androgens are important for the development of sperm

true or false?

A

true

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15
Q

males continue to produce sperm throughout their life. What is ADAM’s syndrome?

A

androgen deficiency aging males

-with age, males slow down (because androgens are important for the development of sperm)

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16
Q

where are leydig cells found?

A

they lie within the interstitium between seminiferous tubules

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17
Q

what does testosterone do?

A
  • influence the reproductive system prior to birth
  • influence sex-specific tissues after birth (requires LH stimulus)
  • additional reproductive effects
  • development of secondary sexual characteristics
  • non-reproductive actions (ex: link in terms of aggression and testosterone levels)
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18
Q

biological effects of testicular androgens

A

prepubertal:

  • accessory sex glands - wolffian duct differentiation and growth
  • external genitalia - growth and differentiation (scrotum and penis)

pubertal:

  • skeleton and muscle - masculine physique, epiphyseal closure
  • vocal cords - voice deepening
  • skin - facial hair growth and/pr cranial hair loss
  • testis - sertoli cell maturation and androgen binding protein synthesis
  • external genitalia - penile and scrotal growth
  • accessory sex glands - prostate, seminal vesicle and bulbourethral growth
  • CNS - libido
  • hypothalamus/pituitary - inhibition of LH secretion (negative feedback)
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19
Q

spermatogonia

A

-undifferentiated germ cells containing a diploid complement of 23 pairs of chromosomes (1 paternal and 1 maternal)

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20
Q

spermatozoa

A

fully differentiated sperm cells containing a random haploid set of 23 chromosomes

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21
Q

what are the 3 key steps in the process of spermatogonia turning into spermatozoa. what happens if something goes wrong during this process?

A

mitotic proliferation, meiosis, and packaging

-sertoli cells scavenge redundant material from these cells, so if something goes wrong they usually catch it

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22
Q

males produce up to _____ sperm cells on daily basis, a lot of energy is required for this.

A

200 million

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23
Q

spermatid development

A
  • meiotic division and the development of the secondary spermatocyte crossing over occurs between paired chromosomes
  • the cytoplasm of spermatids is always joined until complete differentiation and sperm development has occurred
  • half the spermatids have an X and half have a Y
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24
Q

why is it that the cytoplasm of spermatids is always joined until complete differentiation and sperm development has occurred?

A

the X chromosome contains essential elements for spermatogenesis

  • they have to be joined until this differentiation is complete because of the genes on the X chromosomes
  • Y would die without X
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25
Q

what are the 4 main parts of the sperm

A

1) head - nucleus with DNA
2) acrosome - enzymes
3) mid-piece - mitochondria rich
4) tail - swimming

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26
Q

6 roles of sertoli cells

A

1) protect sperm cells
2) feed sperm cells
3) remove unwanted material (when there are malfunctions)
4) secrete seminiferous tubule fluid (high in K+)
5) ABP secretion (does not dissolve readily in water
6) endocrine feedback regulation - inhibin

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27
Q

what is the male reproductive endocrine axis called

A

hypothalamic pituitary gonadal axis

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28
Q

___ targets sertoli cells primarily and ___ targets leydig cells

A

FSH, LH

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29
Q

______ initiates the production of gonadotrophic hormones (FSH and LH)

A

GnRH (from the hypothalamus)

LH and FSH from anterior pituitary

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30
Q

______ will feedback to the anterior pituitary and negatively affects the release of LH and FSH

A

testosterone

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31
Q

____ converts androgens to estrogens

A

aromatase

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32
Q

there are no ____ receptors on male germ cells, this is why estrogen is more present in females

A

androgen

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33
Q

testosterone can bind to estrogen receptors

true or false?

A

false, testosterone will not bind to estrogen receptors but may be converted to a weaker androgen that could bind to estrogen receptors

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34
Q

epididymis (male reproductive tract)

A
  • prior to arriving in the epidydimis, sperm are noon-motile and infertile
  • this concentrates sperm through reabsorption of seminiferous fluid, also protects sperm with defensin

-at the onset of capacitation, sperm obtain the ability to fertilize the egg and become somewhat mobile in the epidydimis (this is completed in the female reproductive tract)

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35
Q

how long do sperm last in the vas (ductus) deferens?

A

storage site can be days in length, longer the storage, less fertile the sperm is likely to be

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36
Q

the ______ empties into the ejaculatory duct

A

seminal vesicles

-this contains fructose, prostoglandins (50% of the seminal fluid), fibrinogen

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37
Q

male reproductive tract accessory glands: contents of the prostate

A

-alkaline fluid, clotting enzymes and fibrinogen

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38
Q

male reproductive tract accessry glands: contents of th bulbourethral gland

A

-mucus like substance

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39
Q

the male sexual act happens in 4 principle phases in humans, what are these phases?

A

1) excitement: arousal and erection
2) plateau phase: continued arousal includes increased heart rate, mean arterial blood pressure, respiration rate and muscle tension
3) orgasmic phase: ejaculation and muscle contraction combined with intense physical pleasure
4) resolution phase: return to pre-arousal state (long in males, short in females)

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40
Q

thoughts about sex or _____ stimuli target higher brain centers, this goes down the descending autonomic pathways (______ stimulation, ____ inhibition), this causes penile arterioles to _______ which causes an erection

A

erotic, parasympathetic, sympathetic, vasodilate

tactile stimulus can also trigger this (mechanoreceptors)
-this follows sensory neurons to the spinal cord and goes up the ascending sensory pathway back to the brain

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41
Q

erection reflex

A
  • stimulation of mechanoreceptors in the gland penis
  • parasympathetic supply to bulbourethral and urethral glands (mucus and lubrication)
  • parasympathetic supply to penile arterioles (penile arteriole dilate, erection, compresses veins)
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42
Q

explain how viagra works

A
  • sildenafil (active ingredient)
  • nitric oxide is released in response to PNS stimulation
  • NO acts through an enzyme linked receptor pathway (second messenger is cGMP)
  • cGMP initiates the PKG pathway (stimulates SR Ca++ ATPase)
  • actin myosin filament interaction is no longer contracting
  • cGMP is degraded by the cellular enzyme phosphodiesterase 5 (target site of viagra)

sooooo, sildenafil promotes longer cGMP life

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43
Q

the ejaculation process happens in 2 phases, what are these phases?

A

1) emission phase: few seconds prior to ejaculation
- sperm moves from vasdeferens to urethra (semen = 10% of total volume)

2) ejaculation: average volume in humans is about 3 ml - can have a substantial range
- average sperm count approx 66 million/ml

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44
Q

what is the criteria for clinically infertile males?

A

when sperm count is less than 20 million/ml

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45
Q

why is the female reproductive system more complicated than the male reproductive system?

A

more complex because it’s not just about gametogenesis - gestation, pregnancy, birth

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46
Q

what are the 2 critical differences in gametogenesis in males and females?

A
  • in females, the number of available gametes is set at birth (conventional view)
  • female reproductive potential ceases in middle age (menopause) - males get andropause but this does not lead to cessation
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47
Q

what is the equivalent of the labia major, minor, and clitoris in the male reproductive system?

A

labia major = scrotum, labia minor = penal shaft, clitoris = penal head/foreskin

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48
Q

oogenesis

A
  • all available gametes usually produced by the fifth month of gestation (cerca 6-6 million) - oogonia but only about 2 million primary oocytes survive at birth
  • meiotic division begins just before birth but is not completed - primary oocytes
  • maintained in a state of meiotic arrest until puberty
  • all primary oocytes are surrounded by a single cell layer known as the zona pellucida
  • the primary follicle encompasses the primary oocyte a single layer of granulosa cells the thecal cells separated by a basement
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49
Q

how long does the ovarian cycle last

A

28 days (ish)

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50
Q

what are the 3 phases of the ovarian cycle?

A

1) follicular phase - preparation of oocyte
2) ovulation - release of secondary oocyte
3) the luteal (postovulatory) ohase: preparation of reproductive tract for pregnancy by hormones from the corpus luteum

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51
Q

the ovarian cycle is interrupted by which 3 things?

A
  • pregnancy
  • menopause
  • nutritional balance, training (amenorrhea)
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52
Q

what is estrous

A

the window where females are fertile - some animals, this can last only days in the year
-during this time there is a massive surge in LH that promote ovulation

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53
Q

lipostat hypothesis

A

delay in puberty in females

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54
Q

what is the uterine cycle? (3 main components)

A

1) menses - beginning of the follicular phase
2) proliferative phase - latter part of the follicular phase (additional endometrial lining laid down)
3) secretory phase - after ovulation during the luteal phase

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55
Q

the uterine cycle is interrupted by which three things?

A
  • pregnancy
  • menopause
  • nutritional balance - training (amenorrhea)
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56
Q

where is the main source of estrogen within females located?

A

theca and granulosa cells

57
Q

follicular development

A
  • theca and granulosa cells begin to synthesize and secrete estrogens
  • follicle increases in diameter - 12-16mm
  • estrogen rich antrum
58
Q

ovulation is controlled by ____ - main target thecal cells and ____ - main target granulosa cells

A

LH, FSH

59
Q

when does the first meiotic division occur in follicular development?

A

just prior to ovulation

60
Q

______ secreted by the follicle allows the mature follicle to break free, the secondary oocyte is expelled into the abdominal cavity and quickly drawn into the oviduct

A

collagenases

61
Q

what is an ectopic pregnancy?

A

when the egg is fertilized somewhere where it shouldn’t be (ex: abdominal cavity) - can be fatal for mother and/or child so pregnancy is usually termianted

62
Q

_____ and ____ cells differentiate into corpus luteum. this synthesizes and secretes mostly progesterone with some estrogens

A

granulosa, thecal

63
Q

in order for the corpus luteum to be able to turn into a mature corpus luteum, which hormones needs to undergo a massive increase?

A

progesterone and estrogens

64
Q

when fertilization does not occur, the corpus luteum turns into _____. this is due to which hormones?

A

corpus albicans
-there is a reduction in circulating levels of progesterone and estrogen, this negatively feedback to anterior pituitary - decreases release of FSH and LH

65
Q

female sexual act in 4 phases

A

1) excitement: arousal and erection increases in PNS and decreases in SNS
2) plateau phase: continued arousal includes increased heart rate, mean arterial blood pressure, respiration rate and muscle tension
- oxytocin levels increase - targets the muscle cells (myometrium) to promote rhythmic contraction within the uterin wall)
3) orgasmic phase: unlike males, this is not essential for successful fertilization, however it does aid in sperm transport
4) resolution phase: if stimulation is sufficient arousal decreases but females do not have a period of latency as in males

66
Q

conception can only take place in a limited window

true or false?

A

true

67
Q

where does conception normally take place?

A

in the distal portion of the fallopian tube

68
Q

sperm can reach the oocyte within ____ minutes following intercourse, but can also survive for up to ____ in the female reproductive tract

A

30, 5 days

69
Q

how does the sperm find th egg once it reaches the female reproductive tract?

A

the oocyte has allurin - hormone that attracts the union of gamete
-it may also follow the temperature gradient (a little warmer in fallopian tube)

70
Q

what aids in sperm travel?

A

-estrogens thinning cervical mucus, estrogens stimulating cervical and oviduct contraction - oxytocin, chemotaxis, thermotaxis

Shortly after ovulation, estrogen is released and will thin mucus and cervical fibers

  • thinning process forms channels within the mucus and fibers
  • these channels are exactly the right size for sperm to swim through, the fibers will also resonate at a similar frequency as the tail frequency of the sperm - sperm that have an irregular tail beat frequency will be blocked (DNA within these sperms may not be good)
71
Q

how long does the sperm take and what percentage of the ejaculation gets to the fertilization site after ejaculation (upper third of oviduct)? the uterus? the cervical canal? the vagina?

A

fertilization site = 30-60 minutes, 0.001% of the sperm

uterus = 10-20 minutes, 0.1 %

cervical canal = 1-3 minutes, 3%

vagina = 0 minutes, 100%

72
Q

acrosomal reaction (fertilization)

A

(once the sperm gets to the egg)

  • acrosomal enzymes allow sperm to “drill” through the corona radiata and zona pellucida
  • fertilin on the sperm membrane binds to integrin on the oocyte surface
  • induces a change in the oocytes membrane which blocks polyspermy (where multiple sperm fertilize an egg)
  • on entry into the cell the sperm releases NO which induces a release of stored Ca++ and this is believed to initiate the final meiotic division in the oocyte
73
Q

is the haploid genome the only thing that the sperm delivers to the egg?

A

-no, sperm also gives NO to the egg, phospholipase C, Ca++, RNA

mitochondrial DNA in sperm is degraded, the mitochondrial DNA we have in us is from our mom

74
Q

zygote formation - syngamy

A
  • sperm and egg plasma fuse
  • sperm nucleus moves into cytoplasm of egg
  • oocyte nucleus completes meiotic division
  • sperm and egg nuclei fuse to form zygote nucleus
75
Q

how rare are twins?

A

-occur in about 1 of every 80-90 pregnancies

76
Q

dizygotic or fraternal twins are the result of _____

A

fertilization of two oocytes

77
Q

monozygotic twins or maternal twins are the result of ______

A

the early embryo dividing in two

conjoined or Siamese twins occur when this division is not complete

78
Q

explain the process of morula all the way to blastocyst

A
  • after about the third day of fertilization - approx. 32 cells = morula
  • inner cell mass will develop into the embryo
  • blastocyst support the cells dividing at the pole during intrauterine life
  • the blastocyst is what fuses to the uterine lining
79
Q

implantation of the blastocyst

A
  • the blastocyst adheres to the endometrium and cells in the trophoblast and begin to digest the surrounding endometrium (releases enzymes that degrade the lining so it can attach)
  • the trophoblast stimulates prostoglandin release: angiogenesis (proliferation of blood vessels), oedema, improved storage
  • the trophoblast will continue to digest the endometrial cells until the placenta develops
80
Q

formation of the placenta

A
  • in approx. 12 days the embryo is completely embedded into the endometrium and the trophoblast is 2 cell layers thick - chorion
  • chorionic villi project into the endometrial spaces filled with maternal blood
  • villi contain embryonic capillaries
  • interlocking maternal (decidual) and fetal (chorionic) tissue = placenta
81
Q

the placenta protects the embryo against many things, and acts as lungs, kidneys, and digestive system but it cannot stop everything, give an example

A
  • alcohol (FAS)

- viruses

82
Q

sex determination in the developing embryo

A
  • each nucleated cell in the human body has 46 paired chromosomes - diploid (except secondary spermocytes and oocytes - haploid)
  • 22 pairs of autosomes and 1 pair of sex chromosomes
  • X and Y
83
Q

what is the sex ratio of a population at fertilization?

A

120 males: 100 females

84
Q

how does the sex ratio at birth differ from the sex ratio at fertilization?

A

at birth, sex ratio is 105 males: 100 females

-therefore, XY has less of a chance of making it to full term

85
Q

what are 4 different unusual karyotypes in sex determination

A

XXY - viable - Klinefelters syndrome - infertile adult males
XYY - viable - no real side effects (super males)
YO - not viable
X0- viable - turner’s syndrome - usually infertile adults

86
Q

for the first ___-___ weeks, XY embryo’s have the potential to go either way; this is called bipotential

A

6-7

87
Q

the sex determining region on the Y chromosome expresses the ____ gene in cells on the urogenital ridge, this stimulates the production of the protein H-Y antigen which directs the development of the male gonads, females of course lack this Y chromosome and therefore lack this gene.

A

SRY

88
Q

the reproductive tract develops from the ____ ducts in females and the _____ ducts in males

A

mullerian, wolffian

89
Q

development of external genetalia

A

1) in the absense of androgens, the external genetalia are feminized

1) DHT (has much higher affinity than testosterone) causes development of male external genetalia
2) the testes descend from the abdominal cavity into the scrotum

90
Q

review of the whole process of sex determination in males

A
  • fertilized by sperm with a Y chromosome, embryo with XY chromosome
  • SRY stimulates production of H-Y antigen in plasma membrane of undifferentiated gonads
  • H-Y antigen directs differentiation of gonads to testes
  • testes secrete mullerian-inhibiting factor which leads to the degeneration of the mullerian ducts
  • testosterone stimulates the release of DHT which promotes the development of undifferentiated external genitalia (penis, scrotum, etc.) and wollfian ducts develop into the male reproductive tract
91
Q

review of the whole process of sex determination in females

A
  • fertilized by sperm with X chromosome, embryo with XX chromosome
  • no Y chromosome, no SRY gene, no H-Y antigen
  • no H-Y antigen undifferentiated gonads develop into ovaries
  • no testosterone or mullerian inhibiting factor
  • absence of mullerian inhibiting factor causes mullerian ducts to develop into the female reproductive tract
  • absence of testosterone leads to the degeneration of wolffian ducts and promotes development of undifferentiated external genitalia (clitoris, labia, etc.)
92
Q

what is the intrauterine position effect

A

rats and mice have bicornate uteruses

  • developing fetuses arranged sequentially in uterine horns
  • each in its own amniotic sac with its own placental connection

-secretions of fetal endocrine glands alter the morphology, physiology, and behaviour of neighbours

-3 types of females, 0M, 1M
,2M
-by 17 days gestation, males have 3X the testosterone of females
-female fetuses are contaminated by testosterone from male neighbours
0hormones pass via uterine blood vessels to neighbouring fetuses can masculinise females

93
Q

what is an example of the intrauterine position effect in humans?

A
  • each male developing into utero increases the probability of subsequent male being gay (maternal immunization hypothesis)
  • mother carrying first son has little exposure to male proteins due to placental barrier
  • mixing of fetal and maternal blood at delivery causes females immune response to male proteins (antibodies produced)
  • subsequent sons are exposed to these antibodies which attack male-specific proteins, thereby altering the development and increasing their chances of being gay (only happens in right handed males)
94
Q

______ stimulates the release of LH and FSH, but too much of this hormone can inhibit the release

A

GnRH

95
Q

too much release of GnRH will inhibit FSH and LH release which is why GnRH acts as a _______

A

pulse generator

-tonic releases of GnRH in both sexes every 1-3 hours

96
Q

which hormones are involved in regulating the pulsatile release of GnRH?

A

norepinephrine and EOP

97
Q

males and females both have a pulse generator and surge generators

true or false?

A

false, they both have pulse generators that regulate the released of GnRH but only females have surge generators that respond to high levels of estrogens (particularly estradiol)

98
Q

effects of sex steroids on gonadotropin release: high plasma estrogen in females

A
  • positive feedback on GnRH
  • increase in GnRH
  • increase in FSH and LH
  • targets the ovaries
  • ovulation
99
Q

effects of sex steroids on gonadotropin release: moderate plasma estrogen in females or androgen in males

A
  • negative feedback on GnRH
  • decrease in GnRH
  • decrease in FSH and LH
  • targets the gonads
  • decrease in estrogen or androgen
100
Q

effects of sex steroids on gonadotropin release: low plasma estrogen in females or androgens in males

A
  • no feedback on GnRH
  • increase in GnRH
  • increase in FSH and LH
  • targets the gonads
  • increase in estrogen or androgen
101
Q

our feedback systems differ for FSH and LH, FSH feedsback to the ____ and LH feedsback to the ____

A

hypothalamus, anterior pituitary

102
Q

in the prepubertal period LH and FSH are not secreted. GnRH secretion begins slowly at the onset of puberty, what sets the wheels in motions for this?

A
  • lip[ostat hypothesis - critical weights (ex: dacner and amenorrhea)
  • gonadostat hypothesis - decreased feedback sensitivity to gonado steroids - GnRH neurons become sensitized, release more GnRH with changes in androgen levels in males
103
Q

steroidogenesis in the follicle

A

2 pathways: delta 4 and delta 5

  • delta 4 pathway: progesterone is quickly synthesized
  • delta 5 pathway: production of androgens
  • steroid synthesis is dominated by delta 4 pathway
  • but in follicular cells, dominant pathway is delta 5
104
Q

how do oral contraceptive work?

A

they are full of progesterone which inhibits the release of FSH and LH from the anterior pituitary

105
Q

how is hormonal control of the ovarian cycle unlike that of the male?

A

1) cyclical in nature
2) FSH and LH do not specifically target gametogenesis or gonadal hormones respectively
3) there are both negative and positive feedback controls

106
Q

during ovulation, why don’t we see the huge surge in FSH like we do in LH?

A

inhibin that is released from ovarian interstitial cells selectively inhibits FSH release - a massive surge in both FSH and LH might target too many follicle that would be developped

107
Q

an increase in the size of a follicle leads to an increase in the production of estrogen

true or false?

A

true

108
Q

GnRH responds to ____ and _____ levels of circulating estrogens

A

moderate and low

109
Q

early follicular phase

A
  • increase in follicle stimulating hormone (FSH)
    • targets the folliculogenesis - approx. 20 follicles that for each given cycle begin that early stage
    • usually only one follicle is ovulated
    • as FSH is released, that promotes development towards an antrol follicle - get stimulation of granulosa cells - largely driven by hormone that is synthesized and released by these cells called growth differentiation factor 9 (GDF9) - target granulosa cells to promote sensitivity to LH
    • LH stimulates P450scc promoting substrate synthesis (androstenediol) - acts as a subsrate for FSH promoting P450scc activity (granulosa cells) - estradiol
    • LH kicks in a little later than FSH to promote growth - estrogens in granulosa cells
    2) at low levels of FSH and LH (early phase) - still operating under that pulse generator - early to mid follicular phase
  • feeds back to pulse generator creating high levels of GnRH vs low level
110
Q

mid follicular phase

A

3) follicle continues to develop (mid to late follicular phase) - increase estrogen levels - point where there is increasing levels of estrogen that feed back to surge generator (closer toward late phase)
- anti mullerian hormone - released from selected follicle - inhibits further development of other follicles during early to mid phase of follicular phase - they do have the ability to synthesize androstenediol - substrate for estrogen synthesis - playing a supporting role for production of estrogens throughout the follicular phase

Inhibin increases in mid to late follicular phase - feeding back selectively to inhibit FSH synthesis and release - to reduce the potential of other follicles to go forward

111
Q

late follicular phase

A

5) Late follicular phase
- surge generator - GnRH increases massively
- we cannot measure in circulation
- positive feedback - estrogens target surge generator that leads to an increase in GnRH and increase in LH, moderate increase in FSH (may be the result in increase in GnRH, increase in inhibin that decreases levels of FSH)

112
Q

ovulation phase

A

6) Ovulation - massive surge in LH
-LH does the following:
A) halt E2 (estrogen) synthesis in follicular cells
B) trigger meiotic division within the egg
C) trigger production of PG’s (prostoglandins)(crucial for rupturing of follicle during ovulation)
D) expansion of cumulus cell oocyte complex
-these secrete matrix metalloproteases (degrade surrounding matrix to make it easier for egg to make it from follicle to fallopian tube)
E) transformation of follicle cells into luteal cells

113
Q

luteal phase

A
  • early luteal phase right after ovulation - estrous (in many primate this phase in obvious)
    • continued inhibition of FSH by inhibin (because don’t want to promote additional folliculogenesis)
    • switch from delta 5 pathway to delta 4 pathway causes rapid increase in progesterone
  • estrogen rises again but does not trigger another surge in LH because progesterone cuts of HPG axis in hypothalamus - inhibition of FSH and LH prevents further maturation of other follicles
114
Q

uterine phase

A

-estrogens drive proliferation of basal endometrium - hyperplasia (lots of cells multiplying) - hyperemia (excessive blood flow)

115
Q

secretory phase

A

progesterone stimulated exocrine production of uterine milk (embryotroph) - nutrient rich source for blastocysts that are not implanted
-progesterone increases mucus secretion in cervix - reduces the chance of sperm entering uterus in possibility that there are sperm already there

116
Q

placental hormones (during pregnancy)

A

human chorionic gonadotropin (hCG): produced by the blastocyst to preserve the corpus luteum. progesterone will inhibit LH release

human placental lactogen: involved with mammary gland development (although not essential) also involved with regulating maternal metabolism - linked with gestational diabetes

117
Q

gestational diabetes (typically type 2)

A

parent offspring conflict - offspring demands nutrients and energy - mother goes into imbalance

118
Q

when does the huge surge in hCG happen?

A

between 1 and 2 months after the beginning of the last menstrual period

119
Q

there is a decline in estrogen and progesterone after parturition (giving birth) in humans

true or false?

A

true

120
Q

how does the concentration of CRH in the blood of mothers during the pre-native state, the normal state, and the late delivery state?

A

highest in pre-native; lowest in late delivery; in between when normal

121
Q

in the US, half of all women will have unplanned pregnancy between the ages of ___ and ___

A

15, 44

122
Q

approximately ___% of unintended pregnancies in the US occur even when contraceptives are used

A

50

123
Q

what are the 3 most effective contraceptive devices?

A
  • intrauterine devices (IUD)
  • contraceptive hormone injection
  • sterilization

these all have a less than 1% chance of getting pregnant

124
Q

how does the combination pill stop contraception?

A

prevents production of a viable egg

125
Q

how does a vasectomy prevent contraception?

A

prevents production of viable sperm

126
Q

how does abstinence, male condom, and coitus interuptus prevent contraception?

A

prevents sperm transport

127
Q

how does tubal ligation prevent contraception?

A

prevents capture of egg by oviduct

128
Q

how do spermicides, diaphragm, cervical cap, contraceptive sponge, and female condom prevent contraception?

A

prevents sperm deposit into vagina

129
Q

how does an intrauterine device prevent contraception

A

prevents union of sperm and egg, prevents implantation of blastocyst in properly prepared endometrium

130
Q

combination pill

A
  • 30 different brads available in North America all contain synthetic estrogen and progesterone
  • typically 2 estrogen types: mestranol or ethinyl estradiol and one of 8 progesterones (ethynodiol diacetate, norethidrone, norethindrone acetate, norethyndrel, norgestrel, desogestral, gestodene, or norgestimate)
  • the combination pill blocks ovulation, conception, and implantation
  • mild and serious side effects as well as benefits independent of their intended use
  • delay in fertility when women come off the pill
131
Q

IUD

A

T-shaped flexible plastic sometimes impregnated with progesterones
-reduces sperm motility and viability, influences development and maturation of the ovum, blocks implantation

132
Q

Diaphragm, sponge, and cervical caps

A
  • used in combination with spermicide

- easily reversible

133
Q

the male “pill”. Why is this not a thing?

A
  • testosterone derivatives have undergone clinical trials but success rates are low in regard to creating infertility (over 40% in caucasian males)
  • androgens alone have significant side effects
  • there are specific calcium channels in sperm tails that could be an option
  • also, because of the fact that males will always be able to reproduce, pharmacies know that they wouldn’t make as much money off of them
  • difficulty marketing males taking estrogens
  • blocking these calcium channels could be the best bet
134
Q

surgical contraception/sterilization

A
  • much more common in females than males
  • tubal ligation - fallopian tubes being tied is reversible
  • hysterectomy - not reversible (removal of ovaries)
  • vasectomy - males version of tubes tied
  • orchidectomy - removal of testes
135
Q

infertility

A
  • considered infertile if after a year of trying there is no pregnancy
  • can be from male (35%) or female (35%) or both (20%)
136
Q

female infertility

A

production of antibodies against sperm or failure to implant developing zygote, blockage, cilliary dysfunction, or endocrine basis

137
Q

male infertility

A

low sperm count, oligospermia, is the leading cause

  • endocrine dysfunction
  • varicocele (varicous veins in the scrotal sac)
  • retrograde ejaculation
  • orchitis (infected testes - can be bacterial, viral, impacts the ability of testes to synthesize fertile sperm)
  • crytorchidism (testes not descending fully during development)
  • impotence
138
Q

in vitro fertilization

A
  • first test tube baby born in bristol, England
  • ovarian stimulation and egg retrieval
  • fertility drugs (gonadotropins) are administered to the woman to stimulate the maturation of several large follicles followed by hCG
  • prior to ovulation 10-12 eggs are removed from the ovary
  • fertilization and embryo transfer
  • sperm obtained from the male and placed in a fluid that nourishes and capacitates the sperm

-the fertilized egg is cultured to ensure normal embryonic development and then inserted into the woman’s uterus

139
Q

there are various means of IVF, what are they?

A

1) when eggs are unable to reach the uterus - internally fertilized
2) woman unable to produce egg - externally fertilized (egg comes from donation)
3) woman unable to produce egg - externally fertilized (surrogate mother)

BIOL 2410 (3 decks)

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