Reproduction Flashcards

(43 cards)

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).

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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

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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
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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
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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).
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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

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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

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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

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9
Q

Maturing Follicle

A

“antral stage”

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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

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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.
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12
Q

fertility drugs

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

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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
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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

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16
Q

ICSI

A

Intra-Cytoplasmic Sperm Injection

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17
Q

“Cleavage”

A

mitosis with no growth

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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
Monozygotic Twinning (2)
Two Inner Cell Masses form - Danger of foetal transfusion syndrome ('twin-to-twin transfusion syndrome)
26
epiblast at top then hypoblast beneath
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
Monozygotic Twinning (3)
Two Primitive Streaks form
28
partial axis duplications
conjoined twins
29
Gastrulation
the node on epiblast has formed. epiblast invaginates to form endoderm some cells touch hypoblast and then rise to form notochord
30
the cns tube
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
neural tube forms above notochord
``` 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
he sealing up of the edges of the tube, and its separation from the ectoderm, sometimes fails:
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
Orofacial cleft
It is treatable surgically
34
Hypospadias
urethra not at end of penis
35
h gigantism
Pituitary tumours are associated with gigantism
36
Growth hormone
e itself affects post-natal muscle growth directly, but other tissues only indirectly.
37
Limb growth is therefore uniquely vulnerable to anything that impairs vascular growth
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
Phocomelia
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
Achondroplasia
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
Your gonads developed in the trunk of your body, about half way between shoulder and pelvis (whatever sex you are).
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
SRY)
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
Complete Androgen insensitivity
this person is | XY
43
guevedoces'
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