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REPRO > REVISION > Flashcards

REVISION Flashcards

1
Q

What are the steps of Spermatogenesis?

A

spermacytogenesis:
spermatogonium –> Type A (remains at basal lamina) and B daugther cells

growth

spermatidogenesis
Type B –> 2 secondary spermatocytes

spermatogenesis
secondary spermatocytes –> early spermatids –> late spermatids –> spermazoa

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2
Q

What is the chromosome and no of homologous strands for:

a) spermatogonium

b) daughter cells s)

c) primary spermatocyte

d) secondary spermatocytes

e) early spermatids

f) late spermatids

g) spermatoza

A

a) diploid 2n 4c

b) diploid 2n 2c 9(after meiosis half number of DNA strand

c) diploid 4c

d) haploid 1n 2c ( meiosis I has occurred)

e) haploid 1n 1c ( meiosis II has occured)

f) haploid 1n 1c

g) haploid s1n 1c

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3
Q

What are the actions of FSH and LH on spermatogenesis?

A

FSH –> acts on Sertoli cells and allows for ABP to sequester testosterone. inhibits inhibin

LH - acts on Leydic cells to release testosterone

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4
Q

describe primary follicles

A

squamous cells become pubertal and get a single layer of cuboidal cells around oocyets

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5
Q

describe secondary follicles

A

multiple layers of cells = granulosa cells

develop receptors for FSH and LH develop so can be stimulated to develop

(begining of ovarian cycle)

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6
Q

what drives the first resumption of meiosis and what occurs at this point?

A

LH surge (associated with ovulation)

LH causes metaphase plate to form and and anaphase to occur

extrusion of the first polar body (1/2 of chromosome compliment) rest remains in functional compliment

diploid 4c –> haploid 2c

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7
Q

what does LH surge do on a follicle level?

A

ruptures follicle = ovulation

lutenising the surrounding ruptured follicle = CL

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8
Q

What cells does LH and FSH act on in ovarian cycle?

A

acts on secondary cells (as prior to this there are no receptors)

FSH: granulosa cells –> converts androgens to estrogens (supports proliferation and fluid accumulation)

LH: thecal cells to produce androgens

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9
Q

What does the corpus luteum secerte and what is needed for it to do so?

A

progetserone, estrogen and inhibin

needs to have LH acting on it

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10
Q

compare gametogenesis in males and females.

A

limit: male= puberty to death, females= limited puberty to menopause

continuity: males = continuos meiosis, females = interrupted meiosis

division: males = 4 (symetrical), females = 1 (asymetric)

cycle= males = asynchronous continuous production, females = monthly production

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11
Q

what substance does the embryo secrete? what is the importance of this?

A

hCG

SB of the embryo secrete this. it is like LH, binds to LH receptor on CL so Progesterone and estrogen production can continue until SB develops into placenta.

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12
Q

What are the three phases of the uterine cycle and what occurs in each of them?

A

menstrual
- P reaches its lowest level = spiral arteries constrict and spasm (starving the endometrium_
- functional layer fragments and sloughs-off as menstrual flow

proliferative:
- rebuilding of functional layer
- high estrogen = thickening of the endometrium and the emergence of spiral arteries and progesterone receptors

secretory: enrichemnt of blood supply and nutrient secretion via endomertial glands (Pe and E support)

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13
Q

what phase of uterine cycle does PCOS put people in constantly and why?

A

persistant, constant level of estrogen puts them in the growth phase (first part of proliferative)

why using COC is important (involves both hormones and ‘sugar pill’ = triggers menstruation

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14
Q

describe relationship between follilce size and estrogen and the impact of this.

A

as estrogen levels increase, the follilce size increases (drives proliferation phase)

when follicle large enough = large amount of estrogen = surge of LH = ovulation and lutenisation of ruptured follicle

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15
Q

describe hormonal control of the proliferative and secretory phase.

A

E increases throughout proliferative phase to macth growing size of follicles. Positive feedback causes a LH and (smaller) FSH surge = ovulation

following ouvulation the CL secrets estrogen and (much more) progesterone. = tissue stops proliferating = secretary = perfect envrionemt for embryo (highly vascular)

FSH and LH start to become supressed

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16
Q

compare P and E levels in pregnant vs non-pregnant cycle

A

Non-Preg:
1-5: E higher than P but relatively constant
5-14 estrogen increases to reach peak, P still low
14- peak for ovulation
15- 20 E declines and P becomes dominant
20- both start to decline as CL degenerates

preg- same untilday 20, as CL is mainatained by the hCG secrted by the baby, E and P coninue to slowly rise.

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17
Q

What happens by day 21 LNMP?

A

embryonic hCG supports CL –> P and E continue

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18
Q

What happens by week 14 LNMP?

A

placental progesterone and oestrogen sufficient to overtake hCG and CL degenerates

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19
Q

Outline the rough outline of embryonic time period?

A

Weeks

0- fertilisation

1- implantation

2- gastrulation

day 17- wk 8: organogenesis

1-12: placemtation

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20
Q

what occurs in week 1 of pregnancy?

A

fertilisation
cleavage and blastocysts formation
blastocyst begins to implant into endometrium

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21
Q

what is needed for fertilisation to be successful?

A

capacitation
- estrogen and vaginal muscus destablise sperm PM and hyperactive motility

acrosome reaction:
P and binding of Zp3 causes increase ca = digestive enzymes from sperm

fertilisation: sperm digest zona and binds to speem-bidning receptor, fuses

polyspermy block: fast (electrical) and slow (cortical granule release and harden zona and remove sperm-binding receptors.

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22
Q

what are the digestive enzymes releasesed in the acrosome reaction?

A

hyaluronidase: penetrates corona radiata

acrosin: digest zona pellucida

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23
Q

outline the steps in pre- implantation development

A

1- Zygote

2- 4 cell stage (2 days)

3- morula solid ball of blastomeres (3 days)

4- early blastocyst (morula hollows out, fills with fluid and hatches from zone pellucida) (4 days)

5- implanting blastocyst- consists if a sphere of trophoblast cells and an eccentric cluster = inner mass (7 days)

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24
Q

what are the week 2 events?

A

implantation completed
placenta and extra embryonic membranes begin development

development of inner cell mass proceeds

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25
Q

what occurs in implantation (not phases)

A
  • trophoblasts bind to and enzymes digest endometrium

-trophoblasts forms cytotrophoblasts (proliferative and different- provide new) and syncytiotrophoblast (secreye hCG, digest and invades endometrium)

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26
Q

Outline the steps in forming the Bilaminar Embryonic disc and Extraembrynoic membranes

A

inner cell mass differentiates into epiblast (clump of cells) ad hypoblasts (underlying, single layer if cells).

epiblasts develop into amnion and hypoblast develop into yolk sac = BILAMINAR EMBRYONIC DISC (epi on top, hypo on bottom)

out-of-pocket hypoblasts and extra-embryonic mesoderm = allantois

extra-embryonic mesoderm + CB and SB = chorion and chorionic villi = beginning of foetal placenta

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27
Q

What occurs in wk 3?

A

appearance of primitive streak
gastrulation- formation fo 3 primary germ layers

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28
Q

describe the formation of the primitive streak

A

primitive streak forms alongs caudal end of bilaminar embryonic disc

first Axis Formation event (forms the head end)

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29
Q

Define gasturaultion

A

epiblasts migrate through primitive streak and form:
- endoderm: displaced cells fo hypoblast
-mesoderm- fill middle-layer
-remaining form ectoderm

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30
Q

what are the week 4-8 events?

A

differentatiation of ectoderm, mesoderm and endoderm

organogensis

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31
Q

How is the placenta matured?

A

extra-embryonic mesoderm lining the CB and SB form the chorion and chorionic villi

chorion and villi of embryo combine with maternal decidua basalis = true placenta

32
Q

What are the placental hormones and their function?

A

hCG: mainatins CL, suppresses immune system

E= enlarges uterus, develops breast and relaxes pelvic ligaments

R= relaxes pelvic ligaments

P= maintains functional endometrium, quietens uterus, develops breasts and increase respiratory tidal volume.

hCS/hPL= decrease glucose and increase FA metabolism, breast development

hCT= increase maternal metabolism

CRH= stimulates cortisol production via foetal HPA

33
Q

when does foetal development begin?

A

week 9

34
Q

What are the overall changes that occur in puberty?

A

8-13 = gradual increase in GnRH (FSH and LH) from pitiuatry = stimulation of oogenesis/ folliculogensis and sex hormone output.

20-fold increase in ostrogen
= stimultaes onset of ovarian and uterine cycles = development of sex organs, external genitalaia and secondary sex characteristics.

35
Q

what is the overall cause of puberty?

A

decreased hypothalamic sensitivity to negative feedback by oestrogen

influenced by maturation of central brain areas (surge centre in females) and elevated levels of leptin, glucose or fatty acids in blood.

36
Q

what is menopause and what is its age of onset?

A

permanent cessation of menstruation (after 12 months of amenorrhea)

52 yrs (avg)

37
Q

What changes occur in menopause?

A

decline in follicles and subsequent fall in oestrogen, inhibin and P

menstural cycle become short, irregular and then long

ultimately ovulation and menstruation ends

38
Q

what are the causes of menopause?

A

decreased H-P axis sensistivety to negative feedback = increase in FSH and LH

rapid depletion of follicles = no oestrogen = anovulation and amenorrhea = menopause

39
Q

what is PCOS?

A

heterogenous disorder of unexplained hyperandrogenic chornic anovulation

40
Q

outline the pathophysiology of PCOS?

A

increased LH –> stimulation of stroma and theca –> increased ovarain androgen secretion –> hyperandrogensism –> increased peripheral aromatisation of androgens –> estrogen

decreased FSH –> decreased follicular maturation –> chronic anovualtion and polycystic ovaries

41
Q

Why are ovarian androgens not converted into estrogen in PCOS?

A

granulosa cells unsupported by decreased FSH

42
Q

describe how insulin resistance occurs in PCOS?

A
43
Q

outline the hormonal profile of PCOS

A

increased: LH, Inhibin, insulin and Estrogen

decreased: SHB and FSH

44
Q

describe the metabolic dysfunction in PCOS.

A

impaired glucose tolerance, dyslipidemia (increased LDL over HDL) and obesity

45
Q

describe the ovarin changes in PCOS.

A

Ultrasound:
-enlarged ovaries
multiple cystic follicles
-hyperplasia of theca

follicle dynamics
-normal dev to mid-antral then arrests
-majority undergo atresia
-granulosa layer thins as follicle enlarges

46
Q

what are the effects of temperature on testicles?

A

Testicular atrophy

Spermatogenic cells atrophy

Leydig cell hyperplasia = increased risk of testicular cancer (T not high due to androgen resistance, low functioning leydig cells and neg feedback)

Only Sertoli cells in SE

47
Q

what are the two phases of testicular descent?

A

Transabdominal
When: First 3-6 months

Hormones: Gubernaculum thickening due to INSL3, testosterone degenerates cranial suspensory ligament.

Inguinoscrotal
When: last trimester (6 months –> birth)

Hormones: shortening and contraction of gubernaculum by testosterone.

48
Q

what is cryptorchidism? (what, treatment, impacts)

A

Incomplete descent in one or both testes

premature babies are at more risk as the inguinoscrotal decent is most likely not to have finished

treated by hCG and earl surgery

leydig cell hyperplasia and spermatogenic atrophy = decreased sperm count

49
Q

What is Varicocele and what is the impact of it?

A

Enlarged spermatic cord veins

Infertility
Reduced blood flow = reduced heat exchange = increased temp = infertility

50
Q

what are the causes of pri and sec hypogonadism and their hormonal profiles?

A

pri
-testicular dysfunction
-klinefelter’s syndrome
increased GnRH

Sec
-pitiurtary dysfunction
-tumour or Kallmann’s syndrome
decreased GnRH

51
Q

What are the causes of hypergonasim?

A

Androgen-secreting tumors

Adrenal adenomas

Leydig cell tumors

52
Q

What are the clinical features of hypergonasim?

A

Precocious puberty

Excessive muscle mass

Mood swings

Unusual body hair growth

Acne

Gynecomastia

53
Q

Explain increased risk of CVD in PCOS

A

High LH: FSH = estrogen levels constantly maintained but still lower than normal (no LH surge or ovulation)

= altered hormone profile means higher LDL:HDL ratio = CVD.

Chornic stimulation of the adrenals including increase cortisol (cardio harmful)

54
Q

Outlines the steps for forming the placenta.

A

mesoderm of CB and SB form the chorion and chorionic villi (three stems: primary, secondary and tertiary). The endometrium then differentiates into the decidua basalis. The chorion and chorionic vili of the foetus combine with decidua basalis to form the true placenta

55
Q

What do trophoblasts differentiate into and what is their respective functions

A

syncytiotrophs (S)
- leading edge of the cell
- produce enzymes that allow embryo to invade the uterine wall
-hCG

cytotrophoblasts(Cy).
-surrounds blastocysts cavity and overlies inner mass.
-allow for the proliferation and differentiation of both cell types.

56
Q

when does the embryonic bilaminar disc form, how is it formed and what does it then go on to create?

A

By the end of day 8.

The inner cell mass of the blastocysts differentiates into epiblasts and hypoblasts.

These form the bilaminar disc and are then used to create the fluid filled cavities.

The leftover hypoblast then invaginate into the allantois w an extraembryonic mesoderm.

This mesoderm along with CBs and SBs form the chorion and chorionic villi of the true placenta.

57
Q

What are the divisions of the broad ligament?

A

mesoarium, mesosalpinx and mesomerism

58
Q

describe the differences between indirect and direct hernias.

A

Direct=
through a weakness and
indirect =
through the inguinal canal.

59
Q

Outline the normal HPA axis

A

GnRH –> LH (–> androgens) and FSH (estrogen)

60
Q

How does the HPA axis change in PCOS? (how does it contribute to insuiln resistance)

A

GnRH –> decreased FSH and increased LH

decreased FSH –> decreased estrogen

Increased LH –> increased androgens –> insulin resistance –> increased BGL –> more insulin-stimulated –> hyperinsuliemia

61
Q

What is the hormonal profile of ovulation?

A

decreased FSH –> increased E (then decline straight after)

increased LH (surge) –> increased androgens

62
Q

Describes what happens to ovulation when someone takes POC and COC?

A

POC:
- increased P = decreased LH (negative feedback) = decreased ovulation

COC
-increased P and E
= decreased LH (by negative feedback)
and thicker cervical mucous

-P = decreased ovulation
E= thick cervical mucous = even more

63
Q

What are the benefits of Estrogen for menopause?

A

increased E =
-increased Ca uptake = bone strength
-increased metabolism
-increased mood.

64
Q

describe the development of the surge centre in males

A

fetal testes produce testosterone –> crosses BBB and become estradiol –> defeminises the brain by inhibiting surge centre development.

65
Q

Describe the development of the surge centre in females

A

a-fetoprotein prevents estradiol from crossing BBB = surge centre development

66
Q

what is the prepubertal GnRH secretion for males and females?

A

pulses of LOW freq and amplitude (tonic centre)

67
Q

What is the post-pubertal GnRH secretion for males and females?

A

both= pulses INCREASE in freq and amplitude (tonic)

females= preovulatory burst (surge centre)

68
Q

compare the secretion of LH for males and females during puberty

A

males= regular low amp, every 2-6 hrs

females= surge ever cycle se[parted by low amp

69
Q

describe the hypothalamus before puberty.

A

tonic centre - HIGHLY SENSITIVE to negative feedback via E and T

surge centre- not yet responsive to E

70
Q

describe the hypothalamus during puberty.

A

Tonic centre: SENSITIVITY DECLINES, increased GnRH

Surge centre: Responsive to POSITIVE feedback by high levels of E

71
Q

what are the earliest changes that indicate the onset of puberty in males vs females?

A
  1. testicular/ scrotal growth
    1. breast budding
72
Q

What is the transitional period to menopause called?

A

climacteric or perimenopause

73
Q

What are the symptoms of perimenopause?

A

menstrual irregularities

hot flushes

mood disturbances (via estrogen fluctuations)

atrophy of repro tracts and breast

bone changes- increased resportion –> osteroperosis

cardiovascular changes: incrased LDL: HDL

74
Q

what age-related changes in the CNS and HP unit may appear in menopausal women?

A

circadian oscillator changes
- decreased nocturnal melatonin
-decreased HP sensitivty to -ve feedback
-gradual rise in LH and FSH

75
Q

summarise the hormonal changes that cause variability in menstrual cycle for perimenopausal women.

A

decreased sensivity of HPA to neg feedback = rise in FSH and LH

increased FSH = recruitment of more secondary follciles

increased E production = accelerated ovulation

ovarian hyperstimulation= no follicle selection and multiple ovulations

accelerated depletion of follicles reverse = decreased cohort size

persistent E = anovulation and heavy menses

few follicles and lower E = anovulation and light menses

anovulation and amenorrhea

76
Q

What is the hormonal profile of a menopausal woman?

A

high LH and FSH )FSH is higher due to loss of neg feedback of inhibin)

low estrogen and inhibin

77
Q

what are the major types of ART and (one sentence) definition

A

AI
-motile sperm IUAI by a catheter

IVF
-ooctye retrived and sperm capacitated, cultured until blastocysts, implanted

ICSI
-incompetent sperm directly injected into oocyte and activated by Ca

ZIFT
-same is IVF but transferred to oviduct not uterus

GIFT
-oocyte transferred into oviduct to bypass blockage

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