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Physiology 1 > Reproduction > Flashcards

Reproduction Flashcards

1
Q

commonalities found between
sexes?

A
  1. Formation of gametes (males and females produce gametes)
  2. Hypothalamic/pituitary control of reproduction
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2
Q

Gametogenesis:
1. Gametes with x chromosomes are produced from cells in the y with z chromosome
2. Mitosis vs Meiosis

A
  1. Gametes with 23 chromosomes are produced from cells in the gonads with 46 chromosomes
  2. Meiosis:
    * DNA replicated once
    * Cells undergo division twice
    * each gamete is haploid
    Mitosis:
    * DNA replicated once
    * Cells undergo division once
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3
Q

Hypothalamic/pituitary control of reproduction

A

1.Internal and enviornmental stimuli in CNS Releases
2. GnRH (gonadotropinreleasing hormone) in hypothalmus which travels to
3. Anterior Pituitary and produces
4. LH = Luteinizing hormone or FSH = Folliclestimulating hormone in the gonads
5. LH goes to endocrine cells and produces steroid and peptide hormones. In females only LH produces gametes directly
6. FSH directly produces gametes

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4
Q
  1. how is GnRH secreted from neuroendocrine cells
  2. low vs high frequency
A
  1. GnRH secreted in pulses from neuroendocrine cells in hypothalamus which tells anterior pituitary to produce LH or FSH. Pulsatility critical for reproductive function. Regulated by hormonal feedback and higher brain centres. Pulse frequency/amplitude changes during development
  2. Low freq= FSH high high freq spike=LH
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5
Q

How are sperm produced?
where?
temperature
how long does it take
how many are produced per day
further muture in

A

Produced in testis in the seminiferous tubule
Optimal at 2-3ºC lower than body temp
Takes ~64 days
200 million/day
Further mature in epididymis

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6
Q

Parts of the seminifurous tubule
2 types of cells and what is Responsible for blood-testis barrier

A

Sertoli cells (sustentacular cells) – Support sperm development
Leydig cells (interstitial cells) – Secrete testosterone
Tight junctions: Responsible for blood-testis barrier. Ensure no immune cells see no developing cells and destroy them because sperm cells are hploid and are diferent

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7
Q

Spermatogenesis
1. when is it formed
2. what happens
3. steps and (n)

A
  1. Spermatogonia:
    * 2n
    * formed during fetal development near basement membrane
    * undergoes mitosis and Following mitosis,
    one spermatogonium stays to produce more
  2. Primary Spermatocytes
    * the other cell begins to undergo meiosis
    forming spermatocytes
    * 2n x 2
    * goes through tight junction towards lumen
  3. Secondary spermatocytes
    * primary spermatocytes undergo meiosis 1 to produce secondary.
    * n x 2
    * secondary go through meisosis 2
  4. Spermatids
    * n
    * four produced from one starting cell
    * Spermatids mature into spermatozoa
    * Lose cytoplasm and gain a tail
    * This is called spermiogenesis
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8
Q

Acrosome
derived from
contains x and y which breakdowns z, a b that covers the a

A
  • derived from the Golgi apparatus
  • contains hyaluronidase and acrosin which
    breakdown the the zona pellucida, a glycoprotein coat that covers the
    oocyte
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9
Q

What is in semen?
Which galnds are exocrine and produce secretion from ducts directly into lumen

A
  1. Spermatozoa (1%) + secretions of accessory glands= Water, Lubricant: Mucous
    Buffers: Neutralize acid, Nutrients: (Fructose, Citric acid, Vitamin C, Carnitine), Enzymes
    Zinc, Prostaglandins: Smooth muscle contraction
  2. Seminal vesicle, prostate gland and bulbourethral gland (secrete buffers)
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10
Q
  1. FSH stimulates x cells which then
  2. LH stimulates x cells which then
A

FSH stimulates Sertoli cells which then
* Support sperm development
* Secrete inhibin
– A hormone that inhibits FSH release
* Secrete androgen-binding protein
– Helps to concentrate androgens in testis
LH stimulates Leydig cells which then
* Secrete testosterone in response to LH

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11
Q
  1. Hypogonadism in XY (decreased fucntion and production of)
  2. Clinical application (2 types)
A
  1. – decreased functional activity of the testes
    – decreased production of androgens,inhibin B, AMH and/or impaired sperm production
  2. a) primary hypogonadism: damage to testes which decreases testosterone but everything upstream is normal (GnRH produced, LH and FSH normal)
    b) Secondary hypogonadism: damage to hypothalmus= decreased GnRH, LH, FSH and testosterone
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12
Q

What does testosterone & related steroids do?
1. Sex-specific tissues (3)
2. Other reproductive effects (2)
3. Secondary sex characteristics (3)
4. Nonreproductive effects (3)

A
  1. Sex-specific tissues
    ❑Promotes spermatogenesis
    ❑Maintains and stimulates secretion from prostate and seminal vesicles
    ❑Maintains reproductive tract
  2. What does testosterone & related steroids do?
    ❑Increases sex drive
    ❑Negative feedback effects on GnRH, LH (and FSH) secretion
  3. Secondary sex characteristics
    ❑Male pattern of hair growth (including baldness)
    ❑Promotes muscle growth
    ❑Increases sebaceous gland secretion
  4. Nonreprodcutive effects
    ❑Promotes protein synthesis
    ❑Increases aggression
    ❑Stimulates erythropoiesis
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13
Q

5-alpha reductase
1. what does it do
2. inhibtors do what

A
  1. turns testosterone into dihydrotestosterone (DHT)
  2. used to treat benign prostate enlargment and male pattern baldness
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14
Q

How are oocytes produced?

Oogenesis
1. During fetal life
2. Before Birth
3. Puberty
4. After puberty
5. Ovulation
6. Fertilization

A
  1. During fetal life, primordial germ cells will go through mitosis to several times to generaloogonia.
  2. Before birth, the oogonia will enter meiosis 1 – duplicate their DNAand STOP – at birth have primary oocytes
  3. Born with ~1 – 2 million primary oocytes.At puberty about 300,000 primary oocytes remain which is the max a woman will ever have
  4. After puberty, one primary ooctye completes meiosisI and enters meiosis II to become a secondary oocyte every ~28 day
  5. The secondary oocyte released at ovulation.
  6. The secondary oocyte completes meiosis II only if it is fertilized (stops in metaphase 2). Dies 12-24 hours after ovulation.
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15
Q

3 Differences between oogenesis and spermatogenesis

A

Oogenesis:
* Asymmetric cell division—only one
secondary oocyte produced from each
oogonium the other is polar bodies
* Limited duration (no oocyte production
after menopause – average age 51)
* Limited number of primary oocytes

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16
Q

oocyte maturation
primary folicles ____
Maturation cycle recruits ____
how many follciles recruited per year
remaining oocytes undergo _______
Granulosa and theca cells role

A
  • girl born with all oocytes in place, approx 0.5 million
  • primary follciles surround oocyte in stasis until puberty
  • maturation cycles recruiyes 5-10 follicles in each ovary only one will fully mature
  • 250 follciles recuirted per year
  • remaining oocytes undergo atresia (hormonlly regulate cell death)
  • Granulosa cells – support oocyte development
  • Theca cells – secrete steroid hormone precursors
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17
Q

Ovarian Cycle:
Phases
parts of each phase (6 parts)

follicular phase

A

Days 1-14: Follicular phase
1. Small # of primordial follicles develop.
2. Become a primary follicle with thecal and granulosa cells. Thecal cells synthesize androgens, which are converted to estrogens in granulosa cells.
3. Some follicles develop to secondary follicles.
4. An antrum (fluid filled cavity forms). Fluid contains hormones and enzymes. Structure now called a tertiary follicle.
5. A dominant (Graafian) follicle develops.
6. The Graafian follicle ruptures and ovulation occurs
- 5- 10 follicles per ovary
- antral fluid contains estrogen and enzymes
- one domiannt follcile selected and remaining follicles die

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18
Q

Luteal Phase

A

Luteal Phase: days 14-28
- Follicular cells left behind in ovary become corpus luteum. Corpus luteum releases progesterone and estrogen.
- If fertilization does not occur, corpus luteum degenerates. The scar tissue remaining is called the corpus albicans.
If fertilization occurs, the corpus luteum continues to make progesterone and estrogen until the end of the first trimester.
1. Dominant follicle ruptures oocyte released into fimbria
2. theca and granulosa cells develop into luteal cells
3. high fat content yellow colour=luteum
4. if oocyte not fertalized degenerates to form corpus albcus

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19
Q

Uterine Cycle
mensus, proliferative phase, secretory phase

A

Menses: (menstrual phase: 1-5) Blood vessels supplying the endometrium undergo constriction causes shedding of the endometrial lining because of declining levels of progesterone and
estrogen.
Proliferative phase: (days 5-14) Endometrium develops in response to estrogen. The endometrial lining thickens as the blood
supply to the tissue is re-established and cells proliferate. Endometrium grows again
Secretory phase: Days 14-28. Glands in endometrium secrete more viscous fluid. Endometrial cells deposit lipid and glycogen in cytoplasm under the influence of
progesterone and estrogen in case oocyte is fertalized

20
Q

Summary of estrogen and progesterone
release during ovarian/uterine cycle

A

Days 1-14: increase estrogen, low progesterone
14-28: continue producing estrogen but slightly lower levels and increase in progesterone

21
Q

Hormonal Control of Menstrual Cycle

Early to mid-follicular phase:
* LH stimulates the release of x from x cells
* FSH stimulates conversion to x by x cells
* x cells also secrete x (anti-Mullerian hormone) prevents recruitment of x
* x exert x feedback on x cells, increasing
x, increasing x
* Estrogens exert x feedback at x and x
* Shut down x and x bc

A
  • LH stimulates the release of androgens from theca cells
  • FSH stimulates conversion to estrogen by granulosa cells
  • Granulosa cells also secrete AMH (anti-Mullerian hormone) prevents recruitment of
    additionalfollicles
  • Estrogens exert positive feedback on granulosa cells, increasing proliferation, increasing estrogen
  • Estrogens exert negative feedback at pituitary and hypothalamus
  • which Shuts down FSH and LH because granulosa is making its own estrogen
22
Q

Hormonal Control of Menstrual Cycle

Late follicular phase & ovulation
* x follicle present
* Follicular cells secrete x, x and x
* Inhibin inhibits x
* x increases pituitary sensitivity to x
* High estrogens increases x pulses to x (x feedback)
* Causes x surge: triggers completion of
x and x

A
  • Tertiary follicle present
  • Follicular cells secrete inhibin, progesterone and estrogen
  • Inhibin inhibits FSH
  • Progesterone increases pituitary sensitivity to GnRH
  • High estrogens increase frequency of GnRH pulses to one every 65 min (positive
    feedback)
  • Causes LH surge: triggers completion of
    meiosis I and ovulation
23
Q

Hormonal Control of Menstrual Cycle

Early to mid-luteal phase:
* Corpus luteum under influence
of x and x releases x, x and
x.
* These hormones exert x feedback at x and x
* Progesterone and estrogen
inhibits x (now one every x)
- LH and FSH do what

A
  • Corpus luteum under influence
    of LH and FSH releases progesterone, inhibin and estrogen.
  • These hormones exert negative feedback at hypothalamus and pituitary
  • Progesterone and estrogen
    inhibits GnRH pulses (now
    one every 3-4 hr)
    LH and FSH drop
24
Q

Hormonal Control of Menstrual Cycle

Late luteal phase:
* The intrinsic life-span of the corpus luteum is
* If fertilization does not take place, corpus luteum
If Corpus luteum undergoes apoptosis:
* x and x levels fall
* Reduced x feedback at x and x returns x
pulses to x
* Causes x and x release

A
  • The intrinsic life-span of the corpus luteum is 12 days
  • If fertilization does not take place, corpus luteum undergoes apoptosis
    If Corpus luteum undergoes apoptosis
  • Progesterone and estrogen levelsfall
  • Reduced negative feedback at hypothalamus and pituitary returns GnRH
    pulses to one every 1.5 hr
  • Causes LH and FSH release
25
Q

Actions of Estrogen
1. Sex-specific tissues
2. other reproductive effects
3. secondary sex characteristics
4. nonreproductive effects

A
  1. Sex-specific tissues
    - promote follicular development and ovulation
    - stimulates growth of the endometrium
    - maintains reproductive tract
  2. other reproductive effects
    - negative feedback effects on GnRH, LH and FSH secretion
  3. secondary sex characteristics
    - stimulates development and growth of breast tissue
    - increases sebaceious secretion
  4. nonreproductive effects
    - promotes fat deposition around hips and thighs
26
Q

Function of Adrenal androgens in afult females
1. other reproductive effects
2. secondary sex characteristics

A
  1. increases sex drive
  2. pubic and axillary (arm pit) hair growth
27
Q

Menopause

A
  • Menopause end of the female reproductive cycle
  • Ovaries lose their ability to respond to FSH and LH
  • Estradiol and progesterone levels fall
  • Lack of negative feedback causes FSH and LH to rise
28
Q

Pregnancy

  1. Sperm deposited in vagina must do what before fertilization
  2. Sperm undergoes x and becomes y
  3. what binds to sperm
  4. what must the sperm pass through
  5. what aids transport
A
  1. Sperm deposited in vagina must mature and travel before fertilization
  2. Sperm undergoes capacitation becomes
    hyperactive (enables swimming motion)
  3. Albumin, enzymes, lipoproteins bind to
    sperm: glycoprotein coat removed intracellular changes develop strong whip-like motion
  4. Sperm must pass through (~30 min)
    cervical mucous (thin, estrogen)
  5. Uterine & oviduct contractions aid transport
29
Q

fertilization:
4. How long is an oocyte and sperm viable for
5. how many soerm reach oocyte and what is it guided by
6. sperm tunnels through what
5. Steps of fertilization (4)
5. what prevents further sperm fusion

A
  1. Oocyte viable for 24h and Spermatozoa viable 4-6 days
  2. About 100 sperm reach oocyte. Guided by chemotaxis (progesterone from cumulus cells that surround oocyte)
  3. Sperm tunnel through barriers (acrosomal enzymes remove the corono radiata)
  4. sperm docks with sperm-binding prtein on oocyte memrbane and triggers oocyte depolarization => Sperm and egg plasma membranes fuse via cortical granules triggering cortical reaction => sperm nucleus moves into cytoplasm of egg=> oocyte nucleus completes meotic dvision=> soern and egg nucleus fuse to form zygote nucleus
  5. coat fertalized ooxyte prevent penetration by addition sperm
30
Q

Fertalization Hormone:
1. WHat is screted from trophoblast
2. takes over from x to maintain x and prevent y
3. similar in structure to
4. basis of what test

A
  1. Human chorionic gonadotropin (hCG) is screted from trophoblast
  2. takes over from pituitary to maintain corpus luteum and prevent next menstural cycle
  3. similar in structure to LH
  4. basis of pregnancy test
30
Q
  1. what does hcg do
  2. what keeps endometrium intact
  3. what three feedback suppression of pituitary
A
  1. hCG maintains the corpus luteum
  2. Progesterone keeps endometrium intact
  3. Progesterone, estrogen, inhibin: feedback suppression of pituitary
30
Q
  1. Placenta roles and exchanges(3)
  2. Placental circulation: linkage, maternal blood forms a, what transfers gases and solutes btwn mother and baby
A
  1. Performs role of Digestive, respiratory and renal systems for the fetus
  2. Exchange of:
    nutrients/waste
    oxygen/carbon dioxide
    proteins, chemicals, etc
  3. Maternal vasculature not physically linked to fetal vasculature
    *Maternal blood forms a lacunae(lake)
    *Fetal chorionic villi transfer gases & solutes between mother & fetus
31
Q

Function of placental hormones

Human chorionic gonadotropin
– maintains —–; stimulates —–
Progesterone
– suppresses ——, ——, —– development
Estrogen
– —- development (x, x, x ), —- development, etc
Human placental lactogen
– Structurally related to —- and —–
– High in —–/low in —–
– Decreases —– uptake of —-, enhances ——

A

Human chorionic gonadotropin
– maintains corpus luteum; stimulates fetal testis
Progesterone
– suppresses uterine contractions, cervical plug, mammary gland development
Estrogen
– uterine development (growth, blood supply, oxytocin receptors), breast duct development, etc
Human placental lactogen
– Structurally related to growth hormone and prolactin
– High in mother/low in fetus
– Decreases maternal cellular uptake of glucose, enhances maternal lipolysis

32
Q

First,second thris trimester, normal birth, preterm, posterm

A

First Trimester: 0-12 weeks after preiod. Embryo development
Second trimester: 12-28 weeks. Fetal development
Third trimester: 28 weeks to delivery. Fetal maturation
Normal Birth: 37-42 weeks
Preterm: Fetus born greater then 28 weeks are viable without intervention
Posterm: greter than 42 weeks. induced or c section

33
Q

Maternal adaptations to pregnancy

Renal:
* increased —- levels increase —
* increased activity — and —–
Cardiovascular: increased —-
* Immune system:
* Calcium homeostasis: x
* x transfer to fetus
* increased x to

A

* Renal:
* increased vasopressin levels increase blood
volume
* increased activity RAS sodium and fluid retention
* Cardiovascular: increased output
* Immune system: partially suppressed
* Calcium homeostasis: pregnancy associated hyperparathyroidism
* calcium transfer to fetus
* increased calcitonin to limit mobilization of
maternal bone

34
Q
  1. How is labour triggered?
  2. Triggers/Intiation
A
  1. Before parturition, relaxin released from ovary and placenta loosens the ligaments in the pelvic bone and cause the cervix to
    soften
  2. Increase estrogen and ocytocin receptors in uterus increase
    - incease fetal cortisol (stress hormon)
    - increase placental corticotropin-releaseing hormone
    - increase prostaglandins
35
Q

hormones are necessary for breast milk:
1. Before parturiton (baby ready to be delivered)
2. after parturition

A
  1. Estrogens and progesterone needed for
    the development of mammary glands but
    inhibit milk production
  2. Prolactin released and stimulates epithelial mil-producing cells
    Oxytocin relased and causes myoepithelial cells to contract
36
Q

Determination of Sex

  1. At 6 weeks: the fetus has a x and y
  2. pathway of x
A
  1. At 6 weeks: the fetus has a bipotential
    primordium (structure that develop based on xxor xy) and rudimentary reproductive
    tracts
  2. XX: Bipotential promordium => ovary => Mullerian duct => fallopian tube, uterus, upper vagina
    XY: Bipotential primordium => y chromosomes => testis => Wolffiam duct => epididymis, vas deferens, seminal vesicle
37
Q

XX: Development of structures
four steps

A
  1. Gonadal corext becomes ovary in the basence of SRY protein and under the infleucne of female-specific genes
  2. Gonadal medulla regresses
  3. Absence of testosterone causes Wolffian duct to degenerate
  4. Absence of anti-Mullerian hormones allows the Mullerian duct to become the Fallopian tube, unterus and upper part of vagina
38
Q

XY genotype

  1. What is so special about the Y chromosome?
A

Has SRY gene that promotes testes development. Encodes a transcription factor; aka TDF (testesdetermining factor)

39
Q

Function of SRY:
4 Steps
what is SF1, SRY, AMH

A

SF1 (Steroidogenic factor 1 transcription factor) in bipotential gonad => SRY (Testesform (note testes DO not need
testosterone to form) => SoX9 => AMH (Anti-Müllerian hormone) Seritoli cells

40
Q

Role of SOX9 in gonadal development:
1. XX vs XY
2. SOX9 initiates what
3. Cellular events downstream of SOX9 does what

A
  1. XY: +SRY = high levels of SOX9 = gonad becomes testis = SRY and SF1 expressed = increase in SOX9 = inhibition of B-catenin
    XX: -SRY= no sox 9 = gonad becomes ovary = b-catenin expressed = inhibtion of SOX9
  2. SOX9 initiates Sertoli cell differentiation
  3. Cellular events downstream of SOX9 rapidly organize testis structure.
41
Q

XY: Development of Structures

4 steps

A
  1. Gonadal cortex regresses
  2. SRY protein in male embryo directs medulla of the bipotential gonad to develop into testis
  3. Anti-Mullerian hormone from testis causes the mullerian ducts to disappear
  4. testosterone from testis converts wolffian duct into seminal vesicle, cas deferens, and epididymis. DHT controls prostate development
42
Q

Variations in sex determination & development

Atypical hormone levels or action:

A

XY – atypical androgen synthesis (e.g., 5-a-reductase) or action
XX – excessive exposure to androgens during early
gestation

43
Q

development in XY individual with complete androgen
insensitivity:
- what happens
Internal structures, external structures, hormone levels

A

development in XY individual with complete androgen insensitivity (androgen receptors not functional) → androgen receptor
not working → no testosteroneaction
Internal structures: Testes undescneded
external structures: Vagina (lower portion, closed end) Infertile, vagina like pouch
hormone levels: Androgens high and LH high

44
Q

puberty:
1. what system is activated
2. what is puberty
3. puberty boys vs girls

A
  1. At the onset of puberty, the GnRH system is activated
  2. Puberty: rapid growth and development
    with earlier, more obvious signs in girls
  3. Boys start later and last longer (between 10 and 20. Girls between 9-14.

Physiology 1 (12 decks)

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