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Flashcards in Reproduction Deck (43)
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1
Q

Spermatogenesis

A

Proliferation of germ line stem cells by
mitosis
• Reduction to haploid state by meiosis
• Differentiation into mature spermatozoa
Mitotic Proliferation.
• Begins at puberty
• Produces (at your age) about 10,000 sperm per
second!
• Typically about 108 sperm / ml of semen.
Mitotic proliferation takes place in the basal side of
the tubule (the side furthest from the lumen).

2
Q

hormonal inputs of spermatogenisis

A

hypothalmus secreted GnRH acting on anterior pituitary which secretes FSH and LH. FSH acts on sertoli cells that stimulate spermatogenisis and inhibit further GnRH secretion. LH acts on leydig cells which secrete testosterone that acts on sertoli cells and reproductive tract organs as well as inhibiting further GnRH release

3
Q

Maturation of sperm

A
Sperm are shed and
flow to the epididymis
The epididymis alters
the seminal fluid
Epididymal secretions
(glycoproteins etc)
activate sperm and
make them capable of
swimming
4
Q

UNLIKE men, adult women have no germ line stem cells

A
Mitosis to bulk up numbers
• Entrance into meiosis
• Pause (for 12-50 years)
• Completion of meiosis
Rate of female gamete production – 13/yr
5
Q

At puberty, the pituitary produces

Follicle Stimulating Hormone (FSH)

A
In response to this, some follicles
resume development (each month, a
surge in FSH causes about 50 more to
do so, throughout the woman’s
reproductive life).
6
Q

Primary follicle

A

During this phase (about 85 days), oocyte grows and
synthesises rRNA and mRNA. It does not progress further
through meiosis

7
Q

Ripening follicle

A

During this phase (10 days), the oocyte synthesises a
glycoprotein zona pellucida, and granulosa cells multiply. Next, granlulosa cells
secrete follicular fluid
that form the fluid-filled
“antrum

8
Q

At a critical stage of the cycle, the developing follicle
depends on receiving a surge of LH from the pituitary
gland; (Thecal cells bind it)

A

If it does not receive this, it dies.
If it does receive it, it matures further to become a Graafian
follicle at the surface of the ovary

9
Q

Maturing Follicle

A

“antral stage”

10
Q

following LH surge

A

primary oocyte completes meiosis 1 and forms a polar body and secondary oocyte that is arrested in meiosis 2
Meiosis II is never completed unless
fertilization happens

11
Q

The remains of the ruptured follicle

become the corpus luteum

A
The Corpus luteum produces hormones
(progesterone, oestrogen) that prepares
the lining of the uterus to receive an
embryo
Unless the woman is pregnant, the CL dies
after a week or so.
12
Q

fertility drugs

A
Exogenous FSH, or
drugs that block
oestrogen detection
and thus drive
higher production of
endogenous FSH,
can stimulate
oogenesis
13
Q

Capacitation

A

Glycoprotein and sterol coat acquired in epididymis is
removed by proteases in the uterine/ cervical fluid.
• This causes the cell membrane to become more
permeable to calcium ions
• These (indirectly, via cAMP) activate strong tail
lashing and make the acrosome reaction possible
later.

14
Q

When sperm meet the Zona Pellucida of the egg,

they undergo an Acrosome Reaction

A
Acrosome
membrane and
plasma membrane
fuse at many
points
Acrosomal contents
spill out and can
digest the zona
pellucida
Fusion causes a
wave of calcium
entry, which keeps
repeating. Calcium waves have two effects;
1 – cortical
granules are
released; these
alter the ZP and
make it
impenetrable by
sperm (and also
block fusion)
2 - Meiosis of the
oocyte resumes
15
Q

Assisted fertilizatio

A

Blocked/ absent oviducts (pelvic inflammatory disease – Chlamydia or
Gonorrhoea often damage oviducts; also congenital absence,
endometriosis of earlier elective tubal ligation).
Blocked vasa deferentia/ eferentia; impotence; low male fertility
Female age

16
Q

ICSI

A

Intra-Cytoplasmic Sperm Injection

17
Q

“Cleavage”

A

mitosis with no growth

18
Q

At the 4 cell stage

A

mRNA synthesis from embryo’s own DNA
begins
maternal mRNA is destroyed at an
increasing rate.

19
Q

2 cell stage, 4 cell stage, morula

A
morula cell mass
trophectoderm
Cells on the inside have contact
all round. Cells on the outside
have a free surface.
This is the first difference, and the
embryo uses it.
20
Q

throphoblast

A

becomes placenta

21
Q

balstocyst

A

hatches through zona pellucida

22
Q

Implantation

A

the trophoblast
of the hatched blastocyst
invades the uterine epithelium

23
Q

All of the cells that make your body

A

now came from your Inner Cell Mass

24
Q

Monozygotic Twinning (1)

A

cells separate inside Z.P.

25
Q

Monozygotic Twinning (2)

A

Two Inner Cell Masses form - Danger of foetal
transfusion syndrome
(‘twin-to-twin transfusion
syndrome)

26
Q

epiblast at top then hypoblast beneath

A

cels at the centre make hex, hex expressing cells move out to tim and congregate at one point. the hex cells release a protein that inhibits progress in epiblast, the cells in epiblast far enough away from hex begin making the tail end of the primitive streak, primitive streak then extends along epipblast and forms a node.

27
Q

Monozygotic Twinning (3)

A

Two Primitive Streaks form

28
Q

partial axis duplications

A

conjoined twins

29
Q

Gastrulation

A

the node on epiblast has formed. epiblast invaginates to form endoderm some cells touch hypoblast and then rise to form notochord

30
Q

the cns tube

A

derives from the ectoderm CNS formation begins when the
ectoderm along the dorsal surface
folds inwards, driven by local cell
shape changes along three stripes;

31
Q

neural tube forms above notochord

A
Much later, cells in the
neural tube send out
processes to each other
and to other structures in
the body. Bundles of such
processes are nerves, and
together the processes
and the cells make the
nervous system
32
Q

he sealing up of the edges of the tube, and its separation from the
ectoderm, sometimes fails:

A

Anencephaly (the inside of the brain is open to
the back of the head: this stops brain growth so
the upper-back head is effectively missing.
Incompatible with post-natal life).
Spina bifida (a very serious case)

33
Q

Orofacial cleft

A

It is treatable surgically

34
Q

Hypospadias

A

urethra not at end of penis

35
Q

h gigantism

A

Pituitary tumours are associated with gigantism

36
Q

Growth hormone

A

e itself affects post-natal
muscle growth directly, but other
tissues only indirectly.

37
Q

Limb growth is therefore uniquely vulnerable to anything that
impairs vascular growth

A

Limb growth has a peculiar vulnerability: it takes place very
rapidly, and makes high demands for oxygen.
It therefore needs the vascular system to grow very quickly into
the elongating limbs

38
Q

Phocomelia

A

It is now known that thalidomide slows
blood vessel growth (it kills developing
blood vessels).
This makes it a valuable anti-cancer drug,
but one
That can only be used safely where there is
no risk of pregnancy.

39
Q

Achondroplasia

A

activating mutation in FGFR3
FGF signalling via FGFR3 usually inhibits
both proliferation and differentiation of
chondrocytes
Activating mutations in FGFR3 cause
growth plates full of chondrocytes, and
premature closure of the growth plates.

40
Q

Your gonads developed in the
trunk of your body, about half
way between shoulder and
pelvis (whatever sex you are).

A

The germ line comes from epiblast cells that were
removed from the body around the time of gastrulation.
It therefore ends up outside the body, in the yolk sac.
The yolk sac has a connection to the gut (endoderm)
The primordial germ cells use this connection, and the gut and its
mesentery, as a way to invade the body;

41
Q

SRY)

A

A gene on the Y chromosome (SRY)
determines sex;
Primitive gonads consist of somatic cells and germ
line cells
• Somatic cells express SRY (if it is present)
• SRY forces somatic cells to develop into testis
cells (otherwise they form ovary cells).

42
Q

Complete
Androgen
insensitivity

A

this person is

XY

43
Q

guevedoces’

A

XY children with deficient 5α-reductase
(‘guevedoces’) therefore make female bodies:
Testosterone itself is a relatively weak
androgen
• Testes secrete testosterone. This stimulates
androgen receptors only weakly
• Tissues - 5α-reductase converts it to 5αdihydrotestosterone
5α-dihydrotestosterone stimulates androgen receptors
strongly
Testosterone rises at puberty
Foetus infant adolescent
This is high enough to act as
an androgen even in the
absence of 5α-reductase