Reproduction Flashcards

1
Q

Why are the testes housed inside the scrotum?

A
  • scrotum/sack outside of body
  • nerves coming down through spermatic cord innervates testes
  • the countercurrent capillary bed that brings in and takes out blood from zone = regulates heat distribution
  • helps heat to be carried away from scrotal sack = keeps testes at least 2 degrees C below core body temp
  • important to house testes inside scrotum = core temp (even 2 degrees C inside body) can be damaging for sperm
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2
Q

Descent of the testes

A
  • lodged way up in the abdominal cavity at about 3 mos
  • starts to gradually move downward through a canal
  • 7 mos = gone down through inguinal canal towards scrotal sac
  • at time of birth = testes should be completely descended or inside the scrotal area

** defects in production of sperm if testes still lodged up in abdominal cavity at time of birth but no problems in hormone production **

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3
Q

Where does sperm production occur?

A

seminiferous tubules
- highly coiled; lead onto network of structures known as the rete testes and then to efferent duct tubes –> epididymis - straight cord up through inguinal canal to become the vas deferens

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4
Q

Cells of the testis: site of sperm and hormone production

A
  • Leydig cells (interstitial cells): secrete testosterone
  • Sertoli cells (epithelial cells): support sperm development
  • smooth muscle (myeloid cells): peristalsis; propel sperm
  • blood-testis barrier: tight junctions; luminal compartment (important for sperm development; stretches from tight junction and goes all the way to inside of lumen); basal compartment (protects luminal compartment; stretches from basement membrane to tight junction = almost like a ring like area to now allow things from outside to get inside the luminal compartment where sperm is being produced)
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5
Q

Functions of the Sertoli cell

A
  1. supports sperm development; “trophic role”
  2. secretes luminal fluid in for sperm housing
  3. secretes androgen-binding protein (androgen buffer, helps maintain steady [androgens] in lumen)
  4. act as target cells for testosterone and FSH (secrete paracrine factors that stimulate spermatogenesis)
  5. secretes inhibin (hormone of negative feedback loop for FSH)
  6. secretes paracrine factors that affect Leydig cell function
  7. phagocytosis of old and damaged sperm
  8. site of immunosuppression (blood-testis barrier)
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6
Q

Effects of androgens

A
  • stimulate spermatogenesis
  • promote development of secondary sex characteristics during puberty and maintenance of these characteristics in adult life
  • increase sex drive
  • promote protein synthesis in skeletal muscle (anabolic)
  • stimulate growth hormone secretion, which permits bone growth during adolescence
  • promote development of male reproductive structures during embryonic life
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7
Q

T or F. Testosterone stimulates erythropoietin secretion from kidneys => goes on to help making RBCs = important action of male hormone

A

T!

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8
Q

Spermiogenesis

A
  • phase included within the process of spermatogenesis
  • last step where spermatids are physically changing to form the sperm
  • physical differentiation, changes in packaging, and cytoplasmic changes
  • ~24 days
  • nucleus = haploid = genetic info along with mitochondria and golgi; small vesicle forms = acrosomal; acrosomal vesicle = enzymes and placed as a cap on top of the nuclear area
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9
Q

T or F. RBCs are bigger than sperm

A

F! Sperm bigger in size than a RBC

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10
Q

Gonadotropins

A
  • FSH: stimulates gametogenesis/spermatogenesis

- LH: stimulates androgen secretion

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11
Q

This is really important to keep access of hypothalamic-pituitary testicular axis active

A

pulsatile secretion of GNRH from hypothalamus (pulses happen every 90 mins for males)
- also causes release of FSH and LH in a pulsatile manner to keep the whole axis active
IF constant level or high dose of GNRH = makes ant pit gonadotrophs insensitive to GNRH and does not keep the axis active

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12
Q

Functions of seminal fluid

A
  1. dilution of sperm
  2. provision of energy (fructose)
  3. formation of semen ‘clot’ (fructose; to help seminal fluid to clot outside body when ejaculate in female tract = protects sperm from being damage)
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13
Q

Seminal vesicles

A

secrete alkaline fluid with fructose, enzymes, and prostaglandins

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14
Q

Prostate gland

A
  • secrete citrate (energy source = antioxidant and to protect sperm lifespan) and enzymes (PSA - anti-clotting factor to break down semen clot (prostate specific antigen); so sperm can then be freed and allowed to move through the female tract)
  • hypertrophy, biomarker for cancer
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15
Q

Bulbourethral glands

A

secrete viscous fluid with mucus

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16
Q

PSA can go up in amount when…

A

there is benign hypertrophy of prostate gland = enlarges and constricts urethra = discomfort and difficulty to void urine!!! = increase in PSA enzyme and can also increase PSA if there is cancerous growth of prostate gland

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17
Q

Neural control of male sexual response

A
  • controlled by autonomic nervous system
  • spinal reflexes (thoracic, lumbar and sacral segments help in coordinating some of the reflexes)
  • phases:
    1. Erection - parasympathetic nervous system
    2. Emission - sympathetic stimulation to the smooth muscles of the ducts
    3. Ejaculation - rapid contraction of skeletal muscle for semen expulsion (somatic control)
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18
Q

200 to 300 mill sperm per ejaculation

So.. what accounts for low # of sperm to reach site of fertilization?

A
  • acidic pH of female tract
  • some sperm don’t have enough E for its swimming/wave-like movement to move through tract so cant go all the way through
  • when semen clot deposited in female cervical area and as the clot starts dissolving and sperm allowed to move upwards through tract, some of it is also lost from female genital tract
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19
Q

Capacitation

A
  • process of sperm maturation that occurs once sperm arrives/deposited in female tract
  • only happens once in environment of female tract!!!
  • ‘destabilization’ of sperm surface membrane (OM)
  • multiple pts on OM = multiple fusion pts are created ; these pts fuse w the membrane of the acrosome - enzyme contained in acrosome released into surrounding which causes sperm head nuclear component to be delivered = happens at time of fertilization
  • before capacitation, tail has wave like movement but once sperm is there in female tract for a while = whiplashing movement (happens during process of activation and allows for proper movement of sperm to site of fertilization)
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20
Q

Site of ova maturation

A

ovaries (female gonads)

  • consists of connective tissue with follicles
  • separate from reproductive tract (they are suspended by ligaments from peritoneal wall)
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21
Q

Female reproductive tract

A

uterus, uterine tubes, vagina

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22
Q

Uterine tubes

A
  • fallopian tubes or oviduct
  • transport ova from ovaries to uterus
  • infundibulum and fimbriae (pick up released ovum)
  • movement of ovum through uterine tube
    > initially = peristaltic contractions
    > mostly ciliary actions
    > duration - 4 days to uterus
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23
Q

Site of fertilization

A

uterine tube

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24
Q

Infundibulum/fimbriae

A
  • finger-like projections like suction cup; sit very close on top of the ovaries
  • after ovum is released during ovulation => suction force develops
  • picks up the released ova into the funnel-like structure and then moves it towards the site of fertilization
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25
Q

What if there is no cilia movement for ovum to move through uterine tube?

A

some fertilized zygote cannot move from site of fertilization to uterus ; needs to move to uterus cuz this is where embryo normally implanted and it will grow into fetus; but if cannot move = zygote can get anchored on the walls of uterine tube and it starts growing there = ectopic pregnancy = not successful preg, not pleasant = uterine tubes don’t have nutrients to support developing zygote/embryo = mom has lots of pain!! has to excise surgically

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26
Q

Site of fetal development

A

Uterus

  • body = upper portion
  • cervix = canal leading to vagina
  • cervix + vagina = birth canal
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27
Q

Wall of uterus

A
  • outer layer = Perimetrium (epithelial cells and CT)
  • middle layer = myometrium (smooth muscle, thickest layer)
  • inner layer = endometrium (layer of epithelial cells, layer of CT, numerous glands)
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28
Q

Ready to expel egg/oocyte

A

Graafian
- once egg ejected out of ovary, the entire follicle becomes empty; if no pregnancy, slowly turns into a small structure and then finally dies off

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29
Q

Menstrual cycle

A
  • 28 days
  • day 1 = first day of bleeding
  • 14 = ovulation, where oocyte will be released from follicle
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30
Q

Follicular phase

A
  • first 14 days
  • when all selected follicles are growing and getting ready for one dominant follicle to ovulate
  • then the next 14 days = luteal phase
  • variable phase; once follicular phase progresses and produces a follicle ready for ovulation, there are hormones that are released - causes lots of changes in the endometrial layer of uterus
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31
Q

T or F. Usually ovarian cycle is 28 days in length but can vary; can be as short as 22 or can be as long as 31/32

A

T!
- no matter the length, the luteal phase pretty much remains constant = from time of ovulation to onset of next menstrual bleeding = LP - stays constant!

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32
Q

Predominant hormone released by follicles on days 1-14

A

estrogen (estrogenic phase)

33
Q

What happens following ovulation (14-28)

A

follicle is converted into endocrine structure called corpus luteum = produces hormones but progesterone predominantly so why this phase called pregestational phase

34
Q

Follicles

A
  • each contain 1 oocyte (primary oocyte stage)
    > starts as primordial follicle; single layer of specialized epithelial cells
  • single layer divides to become more than one layer (granulosa cells)
  • formation of theca cells: interna (closest to granulosa layer) and externa
35
Q

As follicle grows and as a few layers of granulosa cells are formed around the oocyte…

A

this when the connective tissue that surrounds the follicle, they start differentiating and form another layer of cells just around granulosa cell layer ; these cells that originate from connective tissue are known as theca cells

36
Q

After oocyte released, the follicle left behind produces lots of secretions; becomes an endocrine gland

A

corpus luteum; several days of secretions then starts degenerating and shrinking– becomes almost a scar tissue = corpus albicans

37
Q

What triggers loss of corpus luteum function? How does this influence the menstrual cycle?

A

corpus luteum only around when successful pregnancy about to happen – loss of corpus luteum = lack of fertilized ovum ; no pregnancy = demise of corpus luteum function in ovary

38
Q

Folliculogenesis

A
  • FSH exerts mitotic effect on granulosa cells
  • gran cells send out cytoplasmic processes through the zona pellucida and form gap junctions with oocyte
  • nutrients and paracrine factors are extended through these junctions to help the growth of the oocyte
39
Q

FSH effects during early to mid follicular phase (1-7)

A
  • stimulate granulosa cell proliferation, produce E and further growth of antrum
  • increases aromatase synthesis and activity in granulosa cells and more E production
40
Q

Estrogen effects during early to mid follicular phase (1-7)

A
  • further growth of granulosa cells
  • upregulate LH receptors on granulosa cells
  • progesterone receptors on uterine endometrial cells
41
Q

LH receptors on Theca cells

A
  • LH stimulates theca cells to secrete androgens
  • androgens permeate to granulosa cells and converted to E in granulosa cells
  • E secretion rises and dominant follicle is selected
42
Q

Granulosa cells

A
  • secrete anthral fluid
  • provide nutrients for developing oocyte
  • secrete paracrines that support follicle development
  • secrete inhibin
  • secrete E
  • secrete substance that forms zona pellucida
43
Q

T or F. Number of oogonia is fixed prior to birth

A

T, in contrast to males who continually produce spermatogonia

44
Q

Oogenesis

A
  • mitosis starts in the first 2 months of embryonic life
  • meiosis I begins in fetal life
  • meiosis I arrested at 7 mos of fetal life, through birth until puberty
  • 1st meiotic division completed in dominant follicle at time just prior to ovulation
  • meiosis II only completed after fertilization
45
Q

Oogenesis vs Spermatogenesis

A
O = one primary oocyte produces 1 egg (n)
S = one primary spermatocyte produces 4 spermatozoa (n)
46
Q

T or F. Ovarian hormones are not required for female sexual differentiation before birth

A

T!

- required for sexual maturation at puberty and secondary sexual characteristics

47
Q

Proliferative phase

A

uterus prepares for fertilized ovum (estrogens stimulate development of lining)

  • endometrial lining develops; grows
  • endometrial glands enlarge
  • smooth muscle layer thickens
  • cervical glands secrete a thin mucus
48
Q

Secretory phase

A

endometrium prepared for implantation (Progesterone + estrogen)

  • blood supply increased
  • glands enlarge and secrete glycogen-rich fluids
  • cervical secretions more sticky forming a plug
49
Q

Cervix secretes “sperm-friendly” mucus due to

A

Estrogen

progesterone = sperm-unfriendly

50
Q

T or F. Progesterone also increases body temperature

A

T!

51
Q

Timing for fertilization is limited

A

Sperm viable for 5 days

oocyte viable for 12-24 hours

52
Q

Blocks to polyspermy

A
  • change in membrane potential
  • release of contents from cortical granules
  • enzymes enter and harden zona pellucida
  • enzymes inactivate sperm binding receptor
53
Q

At this stage, the fertilized ovum can reach the uterus

A

Morula (3-4 days post fertilization; totipotent up to 16-32 cell stage)

54
Q

Totipotent

A

these cells have the capacity to differentiate to form a complete, fully form human with all the cells and organs needed forming

55
Q

Identical vs. Fraternal Twins

A

IDentical = division of totipotent morula cells

Fraternal = fertilization of two oocytes (released during the same cycle)

56
Q

Blastocyst

A
  • lost zona pellucida and totipotency
  • outer cell = trophoblast; will become placenta; also sticky to help with implantation
  • inner cell mass will become embryo (moved to the side)
  • fluid-filled blastocoele
57
Q

Implantation coincides with which phase of the menstrual cycle?

A

Luteal phase; pregestational
- lots of progesterone is around and so decreases contractility, keeps uterus condition in a calm condition so doesn’t eject implanted blastocyst - prevents early miscarriage or abortion of implanted embryo

58
Q

Which structure creates a barrier b/w blood on mother side and blood on the fetal side to separate blood from mixing between mom and fetus ?

A

epithelial cells of chorionic villus structures and endothelial cells that line the caps coming from fetal side protect from gas exchange occurring across maternal sinus and chorionic villus

59
Q

Human chorionic gonadotropin glycoprotein (hCG)

A
  • placental hormone
  • maintains corpus luteum functions in early pregnancy
  • released from trophoblast cells
  • helps to serve as + indicator of pregnancy bc easily seen
  • peak secretion from almost 60-80 days after last menstrual cycle (then drops sharply for rest of pregnancy)
  • resembles and mimics LH in maintaining corpus luteum functions in pregnancy
60
Q

T or F. Placenta serves as an endocrine gland becomes and produces significantly high amounts of E and P which remains elevated in body

A

T, goes down when placenta expelled from body after childbirth

61
Q

Human chorionic somatomammotropin (hCS) or human placental lactogen (hPL)

A
  • placental hormone
  • GH- like and anti-insulin like actions in the mother
  • helps fetus to avail more glucose
62
Q

E and P as placental hormones

A

P:

  • decreases uterine contractions
  • inhibition of LH and FSH
  • growth of mammary alveolar glands
  • secretes sperm unfriendly mucus

P:

  • growth of uterus myometrium
  • growth of mammary ducts
  • inhibition of LH and FSH
63
Q

Relaxin

A
  • inhibits myometrial contractions (P too)
  • helps to increase blood flow towards uterus during parturition
  • manages renal capacity of mom’s body to accommodate increase in blood vol in mother’s body during pregnancy (regulates glomerular filtration)
  • produced by corpus luteum, then placenta
  • increases cervical ripening
64
Q

Lactogenesis

A
  • initiation of milk synthesis that occurs during pregnancy and lactation (low E and P)
  • prolactin ; need this to maintain lactation
65
Q

This is required for milk ejection or “let-down”

A

Oxytocin
- milk secretion can only happen when prolactin levels rise after parturition is over and E and P have dropped; this is when high prolactin level along w human placental lactogen (some around with growth factors) helps in the process of maintaining lactation

66
Q

Prolactin vs. Oxytocin during suckling reflex

A
  • Prolactin = PRH to anterior pituitary = milk secretion by alveoli in breasts
  • Oxytocin = posterior pituitary; contraction of myoepithelial cells in breasts then milk ejection
67
Q

Klinefelter syndrome

A
  • presence of more than one X chromosome (impairs spermatogenesis)
  • feminine fat distribution, reduced body hair, reduced facial hair, small testes, breast development
68
Q

Turner’s syndrome

A
  • lack of X chromosome
  • streak ovaries: ovaries are there but have ridges on them; no functional follicles; at time of puberty, no menses
  • uterus is not developed
69
Q

Mullerian inhibitting hormone

A
  • secreted by testes from Sertoli cells

- causes regression of Mullerian duct, thereby causing regression of female internal genitalia

70
Q

T being converted to dihydrotestosterone during fetal development

A

DHT causes masculinization of male external genitalia

- testosterone = male internal genitalia

71
Q

T or F. During embryonic development, two ducts are found inside the growing fetus = Mullerian duct and Wolffian duct

A

T, M = female (default) and W duct = male

72
Q

Sexual differentiation in females

A
  • absence of MIH allows Mullerian duct to grow into female internal genitalia
  • absence of testosterone prevents Wolffian duct development so no male internal genitalia
  • absence of DHT = no masculinization of external genitalia
73
Q

Bipotential genitalia

A
  • if testes present –> WD develops to become epididymis, vas deferens and sem vesicles (internal male structures)
  • in absence of testes -> MD grows -> uterus, oviduct/fal tubes, etc.
74
Q

DHT helps in the development of …

A

penis, scrotum and PROSTATE

75
Q

Presence of SRY gene on the chromosome leads to

A

primordial gonads and differentiation into fetal testes = Sertoli and Leydig cells release MIS and testosterone
- if XX = no SRY gene = fetal ovaries (default)

76
Q

Peak rise of testosterone shortly after birth

A
  • known to contribute to development of brain and the effects of this testosterone on brain is brought about by conversion of male hormone to another form of steroid = estrogen
  • testosterone exerts its function in the brain by being converted to estrogen; done by aromatase
77
Q

Complete androgen insensitivity syndrome (CAIS)

A
  • mutation of androgen receptor
  • should bind to androgens but bc of mutation does not bind or respond to androgen on the target tissue; testes present and from there Sertoli sells give rise to MIH which causes regression of MD so no external female structures; Leydig = testosterone, and bc WD has mutations of the receptors , cells of WD duct do not bind and do not respond to testosterone = WD do not develop and no male internal structures as well.. Testosterone converted to DHT; external tissues that supposed to turn into external genitalia also have androgen receptor mutation so do not respond to DHT normally so bc of this – no male structure produced and female external genitalia develops by default (ALTHOUGH testes is present)
78
Q

CAIS symptoms

A
  • 46 XY
  • female external genitalia
  • body female-like
  • breasts develop
  • androgens are converted to estrogen in target tissues
  • absence of ovaries and uterus, no menstrual cycles
  • infertile
79
Q

Congenital adrenal hyperplasia

A
  • XX has ovaries, but outwardly male
  • decreased cortisol = increased ACTH = increased adrenal androgens = masculinization of external genitalia
  • too much androgen production in the fetal stage
  • infertile