Reproduction Lectures (8)

Question 1

Why do humans consider themselves advanced over other animals?
Humans are sexually _____.
R1

Answer 1

• we mate for pleasure, not just procreation

- dimorphic: males and females have distinct characteristics determines by genome

Question 2

Male and female sex organs (3 sets of structures)?

R1

Answer 2

gonads: gamete producing organs – testes VS ovaries

internal genitalia: accessory glands and ducts – epididymis, vas deferens, seminal vesicles, prostate VS fallopian tubes, uterus, cervix, upper vagina

external genitalia: external repro structures – penis, scrotum VS labia, clitorus, opening of vagina

Question 3

Sex determination depends on _____. Why is the Y chromosome so small compared to X?
R1

Answer 3

fusion of egg (X always) with sperm and which sex chromosome the sperm contains (X or Y)
*Y has minimal genes on it, only carries male sex characteristics

Question 4

Since the X chromosome has more genes on it compared to Y, is there a genetic imbalance b/n males and females?
R1

Answer 4

After development of ovaries in females, once X chrom is essentially “shut off” to balance with males

• only thing left on “shut off” X is pseudoautosomal regions at ends which would essentially match a Y chromosome
• whether paternal or maternal X is shut off differs in each cells: this is shown with cats of 2 colours

Question 5

Why does X-linked recessive genetic disorders more commonly affect males?
R1

Answer 5

only need 1 X for it to show, compared to women who need 2 X’s to show it. *Females most often carriers

Question 6

Abnormal sex chromosome distribution during Meiosis?

R1

Answer 6

by end of 2nd meiotic division, should end with 4 monosomic gametes. if not, have nondisjunction:

1. 1st meiotic division ends with all going into 1 cell, by end of 2nd division, have 2 disomic gametes and 2 nullisomic gametes
2. if nondisjunction only occurs at 2nd meiotic division, end with 2 normal monosomic gametes, 1 disomic gamete and 1 nullisomic gamete

Question 7

Products of abnormal sex chromosome distribution during meiosis (syndrome’s)?
XXY, X, XXX, XYY, Y
R1

Answer 7

• XXY (Klinefelter’s): one disomic gamete fertilizes a normal monosomic gamete, extra X causes some female characteristics to form - tall stature, small testes, female-type pubic hair, osteoporosis, breast development sometimes, bad beard growth, infertile
• X (Turner’s): nullisomic gamete fertilizes a normal monosomic gamete, missing pseudoautosomal region of 2nd X - short, neck webbing, broad chest, widely spaced nipples, streak ovaries, infertile, amenorrhoea, pigmented nevi (moles)
• Y: non viable
• XXX: no real phenotypes, 2 X’s inactivated - correlated with learning disorders
• XYY: no real phenotypes, few genes on Y anyway so extra doesn’t affect much - correlated with learning disorders

Question 8

After fertilization (union of egg and sperm) \_\_\_\_\_ forms. Then, \_\_\_\_ followed by \_\_\_\_.
R1

Answer 8

Zygote. Then, blastocyst (3 weeks after fertil, followed by embryo, and eventually fetus (9 weeks after fertilization)

Question 9

Difference between gestational and developmental timeline?

R1

Answer 9

Gestational starts from 1st day of last period (so it’ll be 2 weeks ahead of developmental) = 40wks

Developmental starts when fetus begins developing = 38wks (fertilization length)

Question 10

Internal sex organ development in males and female embryos?

R1

Answer 10

Begins 7th week of development, before this embryo is bipotential
DEPENDS ON PRESENCE/ ABSENCE OF SRY GENE VIA Y CHROMOSOME: females are default essentially

Bipotential gonda: outer cortex and inner medulla
Accessory ducts: mullerian and wolffian

MALE: cortex regresses and medulla forms testis. Mullerian regresses (AMH present) and wolffian forms epididymis, vas deferens, seminal vesicles (testosterone present).
FEMALE: cortex forms ovary and medulla regresses. Mullerian becomes fallopian tube, uterus, cervix, upper 1/2 of vagina and wolffian regresses.

Question 11

How does the SRY gene guide male internal genitalia?

R1

Answer 11

Sex determining Region of Y (SRY) chromosome produces testis determining factor (TDF; transcription factor) which guides development of gondal medulla into testis
-SRY gene takes up large portion of Y chrom

Testis then produce,

• anti-mullerian hormone (AMH or MIS; sertoli cells)
• testosterone (leydig cells): cause proliferation/growth of wolffian into male accessory structures
• testosterone converted to dihydrotestosterone (DHT; leydig cells) to cause external genitalia differentiation

Question 12

External sex organ development in males and female embryos?

R1

Answer 12

after internal has developed
DRIVEN BY PRESENCE/ABSENCE OF ANDROGENS (DHT) MADE BY SRY GENE

bipotential genital tubercle, urethral groove, urethral fold, labioscrotal swelling

if female: genital tubercle forms clitorus, urethra folds and groove forms labia minora, opening of vagina and urethra, labioscrotal swellings form labia majora

if male: genital tubercle forms glans penis (head), urethra folds and groove forms lower portion of penis shaft, labioscrotal swellings form initial portion of shaft and scrotum
**at birth, testosterone causes descent of testes from abdominal cavity into scrotum.

Question 13

What is the testis determining factor?

R2

Answer 13

Y chromosome SRY gene product - testosterone -> DHT is what converts medulla into testes

Question 14

Dihydrotestosterone (DHT) importance came to light how?

R2

Answer 14

during studies of male pseudohermaphrodites who had a defective gene for 5a-reductase, the enzyme converting testosterone to DHT

• had testosterone, but no male external genitalia and prostate development since no DHT
• look female at birth (external genitalia does not develop)
• at puberty the testes secrete testosterone causing masculinization of external genitalia so male can chose which gender they want to be here

Question 15

Male and female gametes?

R2

Answer 15

ovum: largest cell in body; non-motile so smooth muscle contraction and cilia move it; born with all oocytes will ever have, cyclically released during repro years (~40 years)
sperm: small; only flagellated cells in body; move far distance in female repro tract; continually produced for entire life once reached repro maturity; sperm and testosterone production diminish with age but don’t stop

Question 16

Meiosis basic overview: 4 STEPS?

R2

Answer 16

1 - mitosis in utero to inc number of germ cells (oogonia or spermatogonia each with 46 chrom)

2 - DNA replicates but no cell division occurs, still 1 cell with 2 pairs of sister chromatids (homologous pair of replicated diploid chromosomes)= 92 chrom: 1º gamete

3 - first meiotic division, the one 1º gamete divides into 2 seperate 2º gametes (both diploid/sister chromatids, 46 chrom in each cell)

4 - 2nd meiotic division occurs, the 2º gametes both divide to end with 4 haploid daughter 3º gametes

*end with 4 viable gametes if male, in females only 1 will be viable (polar bodies)

Question 17

Female gametogenesis?

R2

Answer 17

germ cells = oogonia

• mitosis (step 1) and the first stage of meiosis (step 2) occur during 5th month of fetal development so by birth, have all 1º oocytes (92 chrom) will ever have
• 5th month have 5-7 million oocytes
• meiosis resumes at puberty with cyclical recruitment of 1º oocytes to enter menstrual cycle
• 1st meiotic division (step 3) produces 1 large 2º oocyte (diploid) and tiny polar body
• ovary releases this diploid 2º oocyte and will not undergo the division unless fertilized
• 2º oocyte begins 2nd meiotic division (step 4) and polar body breaks down during ovulation
• if not fertilized, is released out of body. If fertilized, undergoes the division (step 4) to yield 1 haploid gamete and a polar body

Question 18

What are polar bodies and why are they non viable?

R2

Answer 18

uneven division in cytokinesis yield polar bodies with very little cytoplasm and few organelles, unable to thrive
- uneven distribution comes from the female gamete needing all necessary cytoplasm/proteins/organelles/energy for the zygote as sperm only supplies some DNA

Question 19

Both male and female gametogenesis is under control of _____.
R2

Answer 19

hormones from brain (signalling cascade) and endocrine cells in gonads

Question 20

Male gametogenesis?

R2

Answer 20

• small amnt of meiosis occurs in fetal development to inc immature germ cell numbers (spermatogonia) in testes
• at puberty: germ cell mitosis (step 1) resumes
• some spermatogonia will remain as immature germ cells and continually make more sperm (stay in mitosis step)
• some spermatogonia are recruited to enter cycle to produce 1º spermatocytes (step 2)
• 1º spermatocytes undergo 1st meiotic division to produce two 2º spermatocytes (step 3)
• both 2º spermatocytes undergo 2nd meiotic division to produce 4 immature spermatids (step 4)

All 4 viable

Question 21

How does the brain direct reproduction?

R2

Answer 21

• peptide hormones from hypothalamus go to anterior pituitary, cause secretion of hormones which go to gonads to cause secretion of sex hormones: androgens (DHT, testosterone), estrogens (estradiol - from testosterone), progesterone (progestin)
• males make primarily androgens: 95% made in testes and 5% in adrenal cortex. Most testosterone is converted to DHT in peripheral tissues - both agonists for androgen receptors but DHT is more potent
• females make primarily estrogens and progesterone: most made in ovaries. Some testosterone made in adrenal cortex

Question 22

Hypothalamic-pituitary gonadal axis (HPG axis)?

R2

Answer 22

control pathway for sex hormones

• gonadotropin releasing hormone (GnRH) released pulsatile-ly in hypothalamus travels to anterior pituitary
• produced either in GnRH or kisspeptin neurons
• cause secretions of 2 anterior pituitary gonadotropins from gonadotropes: follicle stimulating hormone (FSH) and luteinizing hormone (LH)
• FSH and LH act on gonads to stimulate sex hormone production and influence gamete production

Question 23

Precursor for all peptide hormones?

R2

Answer 23

Cholesterol

Question 24

Hypophyseal portal system describes _____. Explain the process.
R2

Answer 24

• describes how hypothalamic hormones reach anterior pituitary
• GnRH neurons release GnRH into capillaries of portal system
• portal veins carry trophic neurohormone to anterior pituitary where they act on endocrine cells
• endocrine cells release their hormones into 2nd set of capillaries for distribution to rest of body

Question 25

Feedback pathways that influence GnRH (and ultimately FSH and LH) release during gametogenesis? What are inhibins and activins?
R2

Answer 25

neg feedback: LH and FSH inhibit GnRH release

• in males high amnts of androgens, prog., estrogens -ve feedback loop to dec GnRH release
• in females its same but with high amnts of estrogen, +ve feedback to inc GnRH

Inhibin: peptide hormone that inhibits FSH producing gonadotropes
Activin: opposite

Question 26

Why is positive feedback loop of estrogen and GnRH needed?

R2

Answer 26

significant role in female repro cycle since more estrogen drives egg release

Question 27

Feedback loop: responses for testosterone, estrogen and progesterone specifically?
R2

Answer 27

testosterone: neg feedback to kisspeptin and GnRH (hypothalamus), and gonadotrope neurons (anterior pituitary)

estrogen/progesterone: neg feedback on gonadotrope neurons (to dec LH and FSH) always, neg or POS feedback on kisspeptin neurons only! GnRH neurons do not have estrogen receptors

Question 28

GnRH release specifics? What happens with GnRH deficiencies?

R2

Answer 28

• pulsatie-ly released from hypothalamus every 1-3 hours in both sexes, until there is a feedback
• low levels of androgens and estrogen = pulsatile release so pulsatile production of LH and FSH and sex hormones
• inhibition starts once levels high unless estrogen is high enough in females to result in ovulation
• in kids with a deficiency, they will not sexually mature since no sex hormone production
• need gonadotropin stimulation in gonads: synthetic GnRH delivered pulatile-ly

Question 29

Why does synthetic GnRH have to be delivered in pulsatile manner?
R2

Answer 29

• constant delivery causes down regulation of receptors in pituitary (resistance)
• gonadotropes stops LH and FSH production
• prevents sexual maturity

Question 30

Pulsatile release of GnRH is regulated by?

R3

Answer 30

hormones (neg feedback loop), stress, circadian rhythm, environmental stimuli

Question 31

Environmental factors influencing reproduction?

R3

Answer 31

best studied in females since monthly cycle showing repro cycle is (ab)normal

• affected by: nutritional status, amnt of physical activity, change of day/light cycles altering circadian rhythm
• “environmental estrogens” can bind and activate estrogen receptors/interfere with binding site (anti-estrogens) e.g. phytoestrogens (soy products, pesticides, toxins, fish since synthetic hormones released into water..)

can influence a developing fetus and affect aggressiveness/docile-ness (not proven in humans yet)

Question 32

Male reproductive structures within/on penis?

R3

Answer 32

urethra: urethra and semen passageway
corpus spongiosum: erectile tissue that surrounds urethra to hold it open during erection (inc blood flow) (protective function)
corpora cavernosa: 2 columns of erectile tissue that cause erection when they fill with blood
prepuce: foreskin; can be removed for hygiene etc.
-some evidence that removing it reduces transmission of HIV and STIs and prevalence of cancer and UTIs

Question 33

Male external genitalia?

R3

Answer 33

penis
scrotum: external sac testes migrate into for sperm production since it needs colder temp

if testes do not migrate into scrotum during 1st year, can become infertile; if not descending, given artificial testosterone to induce movement or are surgically moved

Question 34

Male internal genitalia?

R3

Answer 34

accessory glands: seminal vesicle, prostate, bulbourethral glands = produce secretions making up liquid in semen

vas deferens - tube connecting testes to urethra, empty secretions from accessory glands into urethra to join with sperm

Question 35

Prostate gland?

R3

Answer 35

• most common cancer of men is prostate cancer since its a tissue that grows continuously throughout life so its prone to DNA errors
• urination problems and cancer risk if hypertrophy of prostate tissue
• DHT involved in prostate development so administration of 5a-reductase inhibitor (finasteride) will block/reduce DHT production to shrink prostate tissue
• finasteride can also be taken for balding since DHT shrinks hair follicles

Question 36

Testes are made up of (structures)?

R3

Answer 36

• male gonad: produces sperm and hormones
• pair of ovoid structures ~2.5cm by 5cm
• 1 teste = tough fibrous capsule of 250-300 compartments
• within 1 compartment = coils of 400-600 seminiferous tubules (site of sperm production), blood vessels and leydig cells (lie b/n tubules)
• tubule feeds into epididymis (site of sperm storage and maturation)
• epididymis feeds into vas deferens

Question 37

Seminiferous tubules?

R3

Answer 37

site of SPERM PRODUCTION

• developing spermatocytes stack in columns from outer edge -> lumen
• sertoli cells (main controller of spermatogenesis) in between each column
• outer edge spermatocytes are called spermatogonia, as they proceed inward, become sperm
• outer edge (interstitial space outside tubules) is lined with capillaries and leydig cells: produce testosterone

surrounding the tubule are Myoid cells: epithelial cells that secrete basal lamina layer to keep out large particles but allows testosterone to still enter tubules. i.e. controls internal environment

Question 38

Sertoli Cells?

R3

Answer 38

spermatogonia contain tight junctions with adjacent sertoli cells (and basal lamina) to form a blood-testis barrier b/n tubule lumen and interstitial space to control what enters lumen of tubule, and internal enviro

• so sertoli cells regulate sperm development
• “sustentacular cells” = provide sustenance/nourishment to developing spermatocytes
• produce hormones, growth factors, enzymes for mitosis/meiosis, androgen binding protein which binds testosterone to keep it in the lumen

Question 39

General development of sperm inside a seminiferous tubule?

R3

Answer 39

germ cells resting just inside basal lamina: some stay here to continue mitosis, some move forward as they differentiate in meiosis.

• as more sperm enter meiosis essentially push previous sperm forward into lumen
• sertoli cells tight junctions break and reform around migrating cells
• once reaching the lumen, one spermatogonia will undergo 1st and 2nd meiotic divisions to produce 4 immature spermatids
• spermatids remain embedded in apical membrane while they complete maturation

Question 40

Sperm maturation on apical membrane of seminiferous tubules?

R3

Answer 40

• chromatin/nucleus condenses
• microtubule extension (base of nucleus extends outwards to become flagella)
• acrosome (cap over nucleus) forms, contains enzymes needed for fertilization
• mid-piece (body) is full of mitochondria for ATP (flagella)

this process (spermatogonium -> free mature sperm) takes ~64 days

at this point, unable to swim

Question 41

How do the un-motile mature sperm leave the seminiferous tubules?
R3

Answer 41

pushed out of tubule lumen by other developing sperm and bulk flow of fluids into epididymis
- mature (become motile) in epididymis for ~12 days and hang out here until ejaculation occurs epididymal cells secrete proteins allowing complete maturation

Question 42

Spermatogenesis requires ______ and ______.

R3

Answer 42

gonadotropins (LH and FSH) and testosterone

• FSH binds sertoli cells, they generate paracrines needed for mitosis and meiosis
• FSH secretes ABP needed for bringing testosterone into tubules
• FSH causes sertoli cells to release inhibin, inhibits FSH
• LH targets interstitial leydig cells, they make testosterone, which is an inhibitor of LH and GnRH neurons

Question 43

Inhibition of FSH and LH is mainly through _____.

R3

Answer 43

Inhibin: only FSH
testosterone: only LH, and GnRH neurons in hypothalamus

Question 44

Male accessory glands? What are the secretions made of?

R3

Answer 44

• sperm leaving vas deferens is joined by accessory glands secretions creating semen (99% of semen is secretions)

Secretions: nutrients for sperm, buffers (acidic enviro of vagina, residual acidic urine in urethra), chemicals to inc motility, prostaglandins for motility and contraction, protective secretions e.g. immunoglobulins, lysosomes

Question 45

___ influence primary and secondary sex characteristics. What are the primary and secondary sex characteristics?
R4

Answer 45

androgens – anabolic hormones; receptors are nuclear receptors i.e. act on DNA to promote transcription

primary: internal sex organs, external genitalia
secondary: body shape, facial/body hair growth, muscular development, thickening of vocal cords (voice lowering), behavioural effects (libido, aggression)

Question 46

Why do steroids (which are androgens) increase muscle growth?
R4

Answer 46

receptors are nuclear receptors so they act on DNA to promote transcription which is important in skeletal muscle growth

also works everywhere tho: brain, heart, liver, skin, bones, kidneys

Question 47

Female external reproductive structures?

R4

Answer 47

collectively referred to as vulva
labium majus/majora: similar tissue to scrotum
**labia minora and major protect the other external structures
clitorus: bud of erectile and sensory tissue. “clitoral hood” overtop
urethra: urine
opening of vagina: penis receptacle
hymen: layer of skin outside vagnia partially covering the opening

Question 48

Vagina leads to ____. What is the function of this structure? Anatomy of it’s wall (3 layers)?
R4

Answer 48

cervix (opening of uterus) -> uterus (womb)

uterus is where fertilized egg implants and develops

thin “outer” connective tissue layer = perimetrium
thick middle layer of smooth muscle= myometrium
“inner” glandular layer of epithelial cells = endometrium where blastocyst embeds, what is shed during menstruation, and is needed for expelling a fetus

Question 49

Process of egg and sperm making it to each other/fertilizing? cilia
R4

Answer 49

sperm swim into vagina -> cervix -> uterus -> fallopian tubes to meet egg right outside the ovary

egg is released into fallopian tubes which have 2 layers of smooth muscle, the inner layer of which is lined with cilia. Cilia beats and moves egg from ovary -> fallopian tube where it is fertilized.

Cilia beat to move fertilized egg to uterus for implantation, or expulsion if unfertilized

Question 50

Why are cilia so important in the fallopian tubes?

R4

Answer 50

End up with ectopic pregnancy if no cilia to move fertilized egg into uterus, since sperm meets egg right outside ocary

Question 51

What are fimbriae?

R4

Answer 51

“fingers” of fallopian tubes that drape over top the ovary and move slightly to help/ensure the ovulated egg is drawn into fallopian tube

Question 52

Female Gonad: Job and structures?

R4

Answer 52

Ovaries/follicles: make eggs/hormones

• bit smaller than testes
• thick outer cortex of connective tissue surrounds ovary: site of oocyte production
• inner connective tissue layer (stroma): small central medulla w vasculature, holds everything together

Question 53

Follicle development (i.e. how menstrual cycle starts)?
R4

Answer 53

• birth: 500 000 primordial follicles (1º oocytes with pre-granulosa cells layer surrounding) (step 1)
• puberty: 180 000 primordial follicles **only ~480 released in 40yrs
• cyclical recruitment of primordial cells ~1 year before menstrual cycle starts
• 100s recruited into 1º follicles (more granulosa cells) cuboidal shape (step 2)
• these 1º follicles undergo 1st meiosis into 2º follicles with many layers of granulosa cells, and THECA cell in stroma (step 3)
• 2º follicles develop ANTRUM (fluid filled cavity w enzymes/hormones) = 3º follicles
• ~20 3º enter menstrual cycle, only 1 fully develops (step 4)

Question 54

Growth of primordial -> primary -> secondary -> tertiary follicle is _______ of HPG axis.
R4

Answer 54

Independent
- local cell signalling sub’ made within ovary recruit primordial follicles and develop them over a year period into tertiary.

• once tertiary, then depend on HPG axis (FSH mainly)

Question 55

Ovarian cycle (menstrual cycle)?
R4

Answer 55

*start of period = day 1
– follicular phase (~first 2 weeks): recruitment and growth of ~20 tertiary follicles under FSH direction. By day 7, 19 undergo atresia, end with 1 dominant follicle.

– ovulation (day 14): 16-24h before ovulation, meiosis occurs as LH surges, becomes 2ndary. 2ndary oocyte is released from tertiary follicle into fallopian tubes

– luteal phase: (~last 2 weeks): left behind granulosa and theca cells become luteal (yellow; fat) cells so the ruptured follicle/ovary (no oocyte in it anymore) becomes corpus luteum which produces hormones to maintain endometrium in uterus in case fertilization occurs.
*corpus luteum works for ~10 days, then degenerates if egg is not fertilized and menstruation begins again

Question 56

Uterine (menstrual cycle)?

R4

Answer 56

*start of period = day 1
– menses: (3-7 days) degeneration of corpus luteum, shedding of endometrium and some blood

– proliferative phase: (~7 days): uterus adds new cells to endometrium in anticipation of pregnancy.

– secretory phase: (~14 days): after ovulation, hormones (progesterone) from corpus luteum convert endometrium into thickened secretory structure for blastocyst to survive.
*If unfertilized, superficial endometrium layers are lost during menstruation, cycle restarts.

Question 57

Hormonal control of menstrual cycle (ovarian and uterine)?

R4

Answer 57

menses/start of follicular (day 1-7): high GnRH release (repressed for rest of cycle after this) stimulates FSH and LH release
- estrogen, progesterone, inhibin (inhibits FSH) and anti-mullerian hormone start to be released from ovary

during end of follicular/entire proliferative phase (day 7-14) estrogen is primary controller (inhibit GnRH)

ovulation occurs ~day 14 as estrogen switches to + feedback on GnRH: LH (and FSH) surges *FSH is still inhibited by inhibin

during luteal/secretory phase (day 15-28), progesterone is primary controller some estrogen and inhibin tho

Question 58

Hormones during early to mid follicular phase (week 1)?

R4

Answer 58

during period

• pulsatile GnRH secretion since corpus luteum hormones no longer repress it
• FSH recruits ~20 tertiary follicles for maturation
• LH stimulates theca cells to secrete androgens (androstenedione)
• FSH stimulates granulosa cells to convert androgens to estrogen and secrete AMH to prevent more follicular recruitment
• when estrogen gets high, -ve feedback to anterior pituitary and hypothalamus (less GnRH and LH/FSH), +ve on granulosa cells to inc estrogen
• estrogen begins proliferation of endometrium

Question 59

Hormones during late follicular phase to ovulation?

R4

Answer 59

estrogen peaks
– some follicles undergo atresia, dominant follicle persists
– granulosa cells release progesterone and inhibin
– persistently high estrogen for 1-2 days reverses feedback to become +ve on hypothalamus
– inc GnRH, LH surges more than FSH (inhibin)
– high estrogen readies endometrium and high LH drives ovulation

Question 60

Ovulation process

R4

Answer 60

16-24 H after LH surge
– LH causes 1º oocyte maturation: meiosis resumes, 1st division occurs to 2º oocyte
– mature follicles secrete proteolytic enzymes to breakdown its collagen and connective tissue and release oocyte, as well as secrete prostaglandins to allow oocyte to exit ovary and be swept by fimbriae

Question 61

Hormones during early to mid luteal phase?

R5

Answer 61

– thecal and granular cells transform into luteal cells in atrum, under direction of LH surge
– lipid droplets and glycogen granules accumulate in cytoplasm (yellow colour), and begin to secrete progesterone
– progesterone (and estrogen) levels steadily rise, -ve feedback to hypothalamus and anterior pituitary
– progesterone causes endometrium to become secretory structure in prep for blastocyst, and thickens secretions from cervix (cervical plug preventing bacteria and more sperm)

Question 62

Hormones during late luteal phase?

R5

Answer 62

– corpus luteum (luteal cells) keep producing progesterone and estrogen for 12 days post ovulation
– if fertilized, blastocyst releases HcG to maintain it until placenta forms
– if unfertilized, spontaneous apoptosis of corpus luteum to corpus albicans (white, macrophages digest it) takes 2 days
– progesterone/estrogen drop, GnRH inc, FSH/LH inc
– endometrium sheds as progesterone dec (vessels contract backwards, less O2 and nutrients)
– 14 days post ovulation, menstruation begins
– menstruation is ~40ml blood, 35ml serous fluid and cell debris. ~3-7 days

Question 63

Hormones involved in female secondary sex characteristic formation?
R5

Answer 63

– estrogen: breast development, fat distribution to hips and upper thighs (hips)
– androgens (LH and FSH): pubic and armpit hair, libido

Question 64

Requirements for union of sperm and egg in humans?

R5

Answer 64

– females must have receptacle for sperm to enter
– males but have organ to deposit sperm in receptacle
– cannot occur when resting, male is flaccid (can’t be inserted into vagina), requires penis to stiffen/enlarge (erection)

Question 65

Human sexual response steps? (4)

R5

Answer 65

– 1. excitement: erotic stimuli prepare for copulation ex, in bp, heart rate, respiratory rate
– 2. plateau: changes that started during excitement phase intensify (more blood flow to the penis/clitorus/vagina wall/labia minora, inc heart rate, bp, respiratory rate)
– 3. orgasm: both sexes, series of skeletal muscle contractions (uterus, vagina) accompanied by intense pleasure and continued inc bp, heart rate and respiratory rate
– 4. resolution: parameters return to normal

Question 66

Erection in both sexes is a state of ________. (excitement phase) What are some erotic stimuli?
R5

Answer 66

Vasocongestion (inc arterial blood flow) into spongy erectile tissue which exceeds venous outflow

males: capris spongiosum and corpora cavernosa
females: labia minora, vagina walls, clitorus

stimuli: tactile, sensory, physiological stimuli .. to erogenous zones (sexually stimulated areas)

Question 67

Erection reflex in men?

R5

Answer 67

– erotic stimuli inhibits sympathetic pathway, stimulates parasympathetic input, causing erection via Nitric oxide:
– parasympathetic neurons stimulated and ACh released binds muscarinic ACh receptors on endothelial cells, resulting in NO production, which enters vascular smooth muscle cells, causes relaxation (activates myosin light chain phosphatase)
– 2 cavernosal columns in penis have arteries in the centre which dilate from NO (inc inflow into spongy tissue): amnt of blood coming into arteries exceeds amnt of blood leaving in veins, engorging penis and compressing superficial (outside) veins

Question 68

Movement of semen out of the male body (2 processes).

R5

Answer 68

1 – emission: sympathetic activation of smooth muscle and accessory glands; waves of contraction move sperm out of epididymis, through vas deferens, into urethra where its joined by secretions to make semen
2 – ejaculation: somatic/skeletal muscle contractions; expulsion of ~3ml of semen from urethra out of body via series of rapid muscular contractions in base of penis, accompanied by pleasure.
**these can happen in absence of mechanical stimulation: non-sexual erection during REM sleep

Question 69

Sexual dysfunction? Main cause in men?

R5

Answer 69

inability to achieve/sustain erection, disrupts sex act for both men and women not infertility

in men: erectile dysfunction (diabetes, early warning sign of cardiovasc disease/atherosclerosis, neurological disorders like MS and parkinson’s symptom is ED, stress and anxiety, some drugs all dec NO production)

Question 70

Erectile Dysfunction treatments?

R5

Answer 70

PDE5 inhibitors inhibit the enzyme (phosphodiesterase 5) that converts cGMP back to GMP, thus reducing vascular smooth muscle relaxation

these inhibitors allow for continual cGMP conversion so myosin light chain is activated and more Ca+2 is reuptake-d into SR

Question 71

Female sexual dysfunction is most commonly ______. Treatments?
R5

Answer 71

low sexual desire
– flibanserin helps restore prefrontal cortex control over brains motivation/reward pathways enabling sexual desire: activate serotonin receptors to inc dopamine/norepinephrine during sex to inc reward pathway from sexual desire

Question 72

_____ therapy is sometimes prescribed for postmenopausal women with low sexual desire.
R5

Answer 72

Androgen therapy: drug in trial is Bremelanotide – acts on melanocortin receptor in hypothalamus believed to be involved in upregulating women’s sexual response to appropriate cues

• injected
• more effective vs flibanserin
• first invented by self-tanner in pill form

Question 73

Contraceptives are designed to _____. 3 types of contraceptives?
R5

Answer 73

prevent pregnancy
- 85% of women having regular unprotected sex get pregnant within a year

: abstinence (or cyclical abstinence), sterilization (most effective), interventional methods (barriers, implantation prevention, hormones)

Question 74

Contraceptives: sterilization method for both men and women?

R5

Answer 74

best to be saved for after had kids since not easily reversible

tubule ligation in women: prevent union of egg and sperm by cutting and tying/cauterizing/banding fallopian tubes

vasectomy in males: cuts vas deferens to prevent travel of sperm to penis

Question 75

Contraceptives: Barrier methods? (5)

R5

Answer 75

*ancient egyptians used vaginal plugs to prevent pregnancy!

–diaphragm: silicone cup covering cervix/wall of vagina
–cervical cup: smaller than diaphragm, fits over cervix head
*diaphragm and cervical cup usually have spermicide added to them manually
–sponge: diaphragm but already w spermicide
–condom
–female condom: lines entire vaginal wall and covers cervix

Question 76

Contraceptives: implantation prevention methods? Side effects?
R5

Answer 76

IUD (most successful contraceptive if not sterile): plastic devices that create mild inflammatory reaction in endometrium to prevent implantation of blastocyst, as well as kill sperm

• left in uterus against the walls for 5-12 years
• some wrapped in copper (spermicide)
• some secrete progesterone slowly to inc production of thickened mucus at cervix and reduce endometrial proliferation (dec/stop menstruation)

side effects: pain and bleeding to infertility caused by pelvic inflammatory disease and blockage of fallopian tubes

Question 77

Contraceptives: hormonal treatments basics e.g. goal, history? Types? (5)
R6

Answer 77

• females only
• goal: interrupt HPG axis to dec oogenesis or ovulation
• history: girls take plant concoctions phytoestrogens

: depo injection (every 3mo, progesterone, prevents ovulation)
: vaginal ring (replace every month, releases progesterone/estrogen)
: arm implant
: transdermal patch
: pill (1960s *various combos of estrogen/progesterone to alter hypothalamus/a. pituitary, dec GnRH, inhibit gonadotropin release for ovulation, thicken cervical mucus *depends on brand)

Question 78

Male hormonal contraceptives??

R6

Answer 78

RISUG/VaslGel: vasectomy w/o damaging vas deferens; polymer gel injection into vas deferens to coat the walls and kill passing sperm; reversible with bicarbonate injection; in phase 3 clinical trials, many unanswered q’s

NES-T: gel; rub on back of arms; contains progestins to supress HPG axis to suppress testosterone and sperm production; added testosterone in gel; initial results show complete suppression of spermatogen. in 90% of men; reversible

Vaccines attempted; produce antibodies to sperm

Currently, only male contraceptive is condom

Question 79

Infertility is the inability to ____. Most common cause?

R6

Answer 79

inability to conceive
– *low sperm count: normal is 200 million/ejaculation and only half make it to fallopian tubes; anything under 39 million is low. Usually low testosterone is cause, can be STIs (chlamydia, gonorrhea), prostatitis (prostate inflammation prevent sperm movement into urethra), mumps (testes inflammation)

*can also be abnormal shape (structure) or abnormal motility

Question 80

Another major cause of infertility in men? Minor cause in males and females?
R6

Answer 80

major: varicocele – varicose veins w/n testes; defective valves w/n veins cause pooling of blood and inc in temp which dec sperm number
minor: females or males produce sperm antibodies

another minor: retrograde ejaculation – inner urethral sphincter doesn’t contract, semen doesn’t leave body right, goes into bladder

Question 81

5 types of infertility in women?

R6

Answer 81

– damaged fallopian tubes (STIs, surgery, pelvic tuberculosis) have scar tissue; prevent movement of fertilized egg down or sperm up
– endometriosis: endometrial proliferation outside uterus (can’t exit body) causes scar tissue by ovaries/tubes
– PCOS: higher androgen levels cause frozen follicles on ovaries; can be hypothalamic dysfunction, premature ovarian insufficiency (small primordial follicle pool)
– uterine/cervical disorders: endometrial polyps, fibroid formation around tube entrance so fert. eggs can’t go down
– cervical stenosis: narrowing of cervix after trauma/pelvic surgery

Question 82

Assisted reproductive technology: in vitro fertilization stats? Process?
R6

Answer 82

1st baby born in 70s!
av of 31% success first try, varies with age ... 
≤ 35 = 41-43%
≥ 40 = 13-18%
≥ 45 = ~5%

• female given hormones to stimulate egg production (inc # of 3º dominant follicles)
• many eggs vacuumed out from ovaries
• eggs mixed with mans sperm cells in culture dish to fertilize
• blastocysts put in incubator for 48h
• embryos implanted in females uterus or frozen

Question 83

Assisted reproductive technology: artificial insemination?

R6

Answer 83

• inc # of sperm making it up to tubes
• where sperm is deposited differs …
  •intracervical (ICI)- cheapest, least invasive
  •intratubular (ITI)- most effective
  •intrauterine (IUI)

Question 84

Fertilization requires… step 1: capacitation?

R6

Answer 84

• sperm sheds surface glycoproteins, sterols, CHOs in the cervix/uterus allowing them to swim fast (inc Ca+2 permeability), as well as expose receptors needed to penetrate egg
• response to female substances: albumin, lipoproteins, proteolytic enzymes
• during in vitro, before sperm injected into eggs, they are rinsed to cause this
• egg may produce chemical attractants to aid in fertilization 6-24h after ovulation (why it happens so close to ovary distal region)

Question 85

Fertilization requires… step 2: acrosomal reaction?

R6

Answer 85

1º oocyte ovulates, becomes 2º oocyte. Enters tubes with some granulosa cells attached forming corona radiata layer. Sperm must penetrate it and the inside glycoprotein layer (zona pellucida). 
The acrosome (head) of sperm releases enzymes needed to dissolve cell junctions b/n granulosa cells allowing sperm to squeeze through and breakdown a section of zona pellucida

Question 86

Fertilization requires… step 3: cortical reaction?

R6

Answer 86

after sperm binds receptors on egg (why capacitation is needed), plasma memb’s fuse, initiating cortical.

• prevents polyspermy: makes zona pellucida impenetrable – cortica granules w/n egg exocytose proteolytic enzymes that harden zona
• Then nucleus of sperm is donated, 2nd meiotic division occurs forming 2nd polar body (expelled) and haploid egg. DNA fuses to form diploid zygote

Question 87

Timeline of fertilized zygote–> blastocyst? How does gestational vs developmental dating work?
R7

Answer 87

zygote has 6 days of cell divisions as it proceeds from the fallopian tubes into the uterus, via smooth muscle contractions and cilia in tubes (progesterone directed)
-a week after fertilization occurs, the now blastocyst implants into endometrium

since gestational dating starts on 1st day of last menstrual cycle, by the time fertilization /ovulation occurs, considered 2 weeks pregnant, 0 days developed. When implantation occurs, 3 weeks pregnant, 1 week developed

Question 88

Blastocyst basics?

R7

Answer 88

• 100 cells implanting into uterine wall
• TROPHOBLAST: outer cell layer that surrounds inner cell mass layer, and is what invades the endometrium wall 7 days post ovulation.
• Upon contact w endometrium trophoblasts proliferate and secrete proteolytic enzymes allowing blastocyst to penetrate/bury into wall and throughout development, embryo is completely surrounded by endometrium

Question 89

Trophoblast of blastocyst forms ______. What does the inner cell mass form?
R7

Answer 89

-CHORION = extraembryonic memb enclosing embryo and forming placenta

• forms EMBRYO and other extraembryonic membs:
• AMNION (secretes amniotic fluid existing w/n chorion as a protective cushion for embryo; assists in developing skeletal muscles since embryo can move/float)
• ALLANTOIS (umbilical cord)
• YOLK SACK (serves as circulatory system, absorbs nutrients/subs from amniotic fluid that diffuse into embryo; disappears once placenta forms)

Question 90

How does the placenta form?

R7

Answer 90

• a section of chorion starts to form chorionic villi that penetrate vascularized endometrium that formed in secretory phase of uterine cycle
• chorionic villi have vasculature from embryo
• chorionic villi secrete enzymes that breakdown endometrial walls and maternal blood vessels to allow moms blood to empty into intervillous space and bathe chorionic villi so the embryo gets O2 blood

Question 91

Is there a direct connection b/n mother’s blood and embryo’s blood?
R7

Answer 91

NO

• intervillous space is where nutrients, gases, wastes get exchanged across membs of villi (diffusion)
• umbilical cord has 1 vein bringing O2 nutrient-filled blood into embryo, and 2 arteries carrying deO2 waste-filled blood away from embryo
• placenta grows to 20 cm in diameter and can receive up to 10% of maternal CO – diameter allows more maternal blood to bathe the villi allowing more exchange

Question 92

Human chorionic gonadotropin hormone role?

R7

Answer 92

embedded blastocyst immediately begins secreting hCG to keep corpus luteum intact, since it is needed to maintain endometrium layer

• hCG is similar to LH so it binds to LH receptors in corpus luteum and keeps its hormone secretion going
• hCG initially stimulates testosterone/DHT production in developing testes in male fetuses after 7 weeks
• hCG is hormone detected in pregnancy test since it only starts after blastocysts embeds (3 weeks after menstruation)
• after 7 weeks of DEVELOPMENT placenta is formed and takes over estrogen/progesterone levels, corpus luteum can degenerate

Question 93

When does hCG levels drop during pregnancy?

R7

Answer 93

after placenta takes over since corpus luteum does not need to be maintained

Question 94

Which hormones does the placenta secrete?

R7

Answer 94

• Progesterone/Estrogen: neg feedback to HPG axis prevents follicle development and initiation of another menstrual cycle.
• Estrogen inc # and size of milk secreting ducts in breasts.
• Progesterone maintains endometrium, suppresses smooth muscle contractions to prevent premee uterine contractions
• Human placental lactogen (hPL; human chorionic somato-mammotropin, hCS) is similar to growth hormone and prolactin, alters mother’s glucose and fa metabolism to support fetal growth (dec insulin sensitivity so more glucose uptake into tissues/blood, inc lipolysis so more fa in blood, this ensures more energy available for embryo
• *not for breast development and milk production**

Question 95

Why do 4% of pregnant women have gestational diabetes?

R7

Answer 95

insulin insensitivity due to human placental lactogen (hPL) i.e. human chorionic somatomammotropin (hCS)

Question 96

Parturition process begins with ____. What are the 3 possible initiators of the sudden labour?
R7

Answer 96

birth occurs b/n 38-40th week of gestation
-labor: sudden rhythmic contractions of the uterus myometrium layer

• progesterone and estrogen drop: in some animals, not in humans (doesn’t drop until placenta is removed)
• oxytocin inc: but doesn’t inc in humans until after labour begins used to induce labor
• placenta releases corticotropin releasing hormone: some evidence high enough CRH can cause premee labor

Question 97

Days before labor the ____ softens and ____ loosen. These two events are under ____ control. What is the positive feedback loop in birth?
R7

Answer 97

cervix softens so baby can pass through; ligaments holding pelvic bones together loosen so pelvis can open wider.
These 2 are under enzymatic control: high estrogen/relaxin from placenta

initiation of contractions, fetus pushed lower, pressure on cervix, cervix stretched, sensed by stretch receptor, sends info to MNC receptors in hypothalamus, releases oxytocin, causes more uterine contractions top-bottom and prostaglandin and CRH release, inc force of contractions, baby pushed down ….. contractions gets more forceful and frequent as it continues

Question 98

The structure of a breast mammary gland?

R7

Answer 98

similar to sweat glands

• each gland has 15-20 lobes surrounding nipple
• each lobe has many lobules
• each lobule has many acini/alveoli
• acini surrounded by epithelial milk secreting cells and myoepithelial cells
• smooth muscle lines duct walls
• milk production occurs in acini, ejected into lobular glands and feeds into larger milk ducts to exit breast
• milk contains lots of fats and protein

Question 99

Lactation process?

R7

Answer 99

*puberty: estrogen= milk duct proliferation, fat deposition
pregnancy:
- milk glands develop more w inc estrogen, growth hormone, cortisol, and progesterone converts epithelial cells into secretory structures later on
- high estrogen/progesterone inhibits milk production so milk doesn’t come in until placenta is removed: initially colostrum is made (inc protein, antibodies, immuno’s)

3 days after birth:

• prolactin inc 10fold from anterior pituitary (bc est/prog drops and prolactin inhibitory hormone drops later in pregnancy): stimulates acini cells
• oxytocin causes milk ejection: mechanical activation of sensory neurons in nipples stimulates hypothalamic oxytocin, causes smooth muscle contractions in breast (myoepithelial) and uterus
• can occur w/o pregnancy if higher brain centre is activated e.g. hearing a baby cry

Question 100

Puberty growth?

R7

Answer 100

• quickly in females: breasts bud and period starts, av of 12 years old (range 8-13)
• subtle/slow process in men: growth/maturation of genitalia, pubic and facial hair, voice lowering, inc in testosterone so height etc. 9-14 years old

maturation of HPG axis occurs: inc in pulsatile GnRH release

• genetically pre-programmed: inheritance patterns w mom/daughter timing of first menstrual cycle
• low adipose tissue in females (leptin) can cause women to miss periods e.g. intense athletes

Question 101

Aging in females (i.e. stopping of period)?

R7

Answer 101

Menopause: ~40yrs after 1st menstrual cycle; ovaries no longer respond to LH/FSH since no more follicles to recruit; absence of estrogen causes hot flashes, osteoporosis etc; must not have had a period for 1 year. Perimenopause is the time leading up to it with infrequent periods.

Question 102

Menopause but in men is _____.

R7

Answer 102

“andropause” - not real
-testosterone dec with age causing less sperm production, energy, lean muscle mass, ability to hold an erection; dec in testosterone due to dec # of leydig cells and responsivity to LH (could be dec HPG axis activity)