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Embryology > Introduction and Gametogenesis > Flashcards

Introduction and Gametogenesis Flashcards

1
Q

What are the periods of human embryology from a medical point of view?

A

1st, 2nd, and 3rd trimester

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2
Q

What are the periods of human embryology from an embryological point of view?

A
  1. Period of the egg: from fertilization to implantation (conceptus or preimplantation embryo); zygote, morula, blastocyst
  2. Period of the embryo: From the implantation (end first week) to the 8th wk
  3. Period of the fetus: from the end of the 8th week of gestation (2nd month after fertilization)
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3
Q

How is pregnancy dated?

A
  1. Fertilisation age: count the weeks to delivery starting from day of fertilisation (difficult to know the exact moment of fertilisation + eggs may survive 2 days in the ovarian tube and spermatozoa 4 days)- in this case pregnancy = 38 weeks
  2. Onset of the last menstrual period: the pregnancy should last 40 weeks. It is hard to assume the Estimated Due Date (EDD) based on the last menstrual period (LMP) because it is based on the assumption of a regular cycle of 28 days.
  3. Crown Rump Length (CRL): by measuring this length in the first trimester through an ultrasound we can determine the gestational age of the fetus
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4
Q

What are teratogens?

A

Chemical, physical or biological agents that alter fetal morphology
or function if the fetus is exposed to it during a critical stage of development.

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5
Q

What are the phases of gametogenesis?

A
  1. Formation of primordial germ cells (PGC) and their migration.
  2. Increase in PGCs by mitosis.
  3. Reduction in chromosome number by meiosis.
  4. Structural and functional maturation of egg and sperm.
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6
Q

How do male and female gametogenesis differ in the timing of PGC activity?

A

Females: PGCs enter meiosis by the 5th month of fetal life and are arrested until puberty.

Males: PGCs remain dormant until puberty, then proliferate continuously throughout life.

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7
Q

What are the key phases of meiosis in gametogenesis?

A

Reduction in chromosome number.

Reassortment of genetic material.

Crossing over during the first meiotic division.

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8
Q

What are the 3 main causes of birth defects?

A
  • Genetics
  • Environmental factors (drugs, viruses…)
  • Multifactorial inheritance (genetic + environmental)
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9
Q

For how many % of birth defects is the cause unknown?

A

50-60

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10
Q

What is migration?

A

a complex mechanisms that requires dynamic rearrangement of the cytoskeleton

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11
Q

What happens during migration?

A

The cell moves by extending the
lamellipodium (actin filaments) which adheres to the extracellular matrix, then the nucleus is
moved and the adhesion is detached.

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12
Q

What is a teratoma?

A

A germ cell tumor that can contain tissues like hair, muscle, or bone. It may form in gonads or extragonadal sites and can be benign or malignant.

They may be mature or immature, based on how
normal the cells look under a microscope. Sometimes
teratomas are a mix of mature and immature cells.

Teratomas usually occur in the ovaries in women, the
testicles in men, and the tailbone in children (sacrococcygeal
teratomas).

They may also occur in the central nervous system (brain or
spinal cord), chest, or abdomen.

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13
Q

At what stage do all oogonia enter the prophase of the first meiotic division?

A

By the 5th month of fetal development.

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14
Q

How many primary oocytes are present at various stages of a female’s life?

A

5th month of fetal development: ~7 million.
At birth: ~2 million.
At puberty: ~40,000.
Ovulated during reproductive life: ~400.

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15
Q

What happens to primordial germ cells (PGCs) in the ovary?

A

PGCs are invested by support cells and become oogonia, which develop into primary oocytes.

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16
Q

What happens to male PGCs (spermatogonia) during the embryonic period?

A

They proliferate during the early embryonic period but become dormant from the 6th week of fetal life until puberty.

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17
Q

What occurs to spermatogonia after puberty in males?

A

They proliferate intensively and continue to do so throughout life, maintaining fertility.

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18
Q

What are the key phases of meiosis in gametogenesis?

A

Reduction in chromosome number.
Reassortment of genetic material.
Crossing over during the first meiotic division.

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19
Q

How many viable gametes form in males and females during meiosis?

A

4 in males, 1 in
females

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20
Q

Why is the completion of meiosis in females described as a “leisurely process”?

A

Because the first meiotic division begins in fetal life and remains arrested at the diplotene stage until ovulation, which may take up to 50 years.

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21
Q

What additional materials are stored during female meiosis for early embryonic development?

A

rRNA
mRNA
Cortical granules

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22
Q

At what stages are the first and second meiotic divisions completed in females?

A

First meiotic division: Completed at ovulation.
Second meiotic division: Completed only if fertilization occurs.

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23
Q

How does meiosis progress in males compared to females?

A

Females: Meiosis is synchronous but slow, with the first division completed at ovulation and the second division completed upon fertilization.
Males: Meiosis is asynchronous and faster, with the first meiotic division lasting 24 days and the second lasting 8 hours.

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24
Q

What triggers male spermatogenesis at puberty?

A

A surge in testosterone leads to:

Maturation of Sertoli cells into seminiferous tubules.
Proliferation of PGCs into spermatogonia.
Development of secondary sexual characteristics.

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25
Q

What are the time frames for spermatogenesis in males?

A

Spermatogonia proliferation: 16 days.
First meiotic division: 24 days.
Second meiotic division: 8 hours.
Spermiogenesis: 24 days.
Total: ~64 days.

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26
Q

What is the function of Sertoli cells in male meiosis?

A

Sertoli cells support spermatogenesis by:

Providing nutrients.
Regulating the seminiferous tubules.
Phagocytosing residual cytoplasm.

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27
Q

What role do Sertoli cells play in spermatogenesis?

A

Maintain the blood-testis barrier.
Support spermatogenesis.
Secrete androgen-binding protein and tubular fluid.
Secretion of other proteins
inhibin and activine for feed-back loop to hypothalamus (FSH), Mullerian-inhibiting factor, Retinal-binding protein

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28
Q

What is the structure of the parenchyma of the testis?

A

The parenchyma of the testis is divided into lobules, each containing one to four seminiferous tubules.

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29
Q

What is the function of the rete testis?

A

The rete testis collects:

Testicular sperm.
Secretory proteins.
Fluid and ions from the seminiferous epithelium.

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30
Q

What types of cells make up the seminiferous epithelium?

A

Support cells: Sertoli cells.
Spermatogenic cells: Mitotically dividing spermatogonia, meiotically dividing spermatocytes, and haploid spermatids.

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31
Q

What structures surround the seminiferous tubules?

A

Basement membrane.
Outer wall: Connective tissue with elastic fibers, collagen fibers, fibroblasts, and myoid cells.

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32
Q

What is found in the intertubular space of the testis?

A

Leydig cells (testosterone production).
Blood vessels.
Lymphatic vessels.
Immune system cells.

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33
Q

What is the blood-testis barrier?

A

The blood-testis barrier is formed by tight junctions between Sertoli cells. It separates the basal compartment from the adluminal compartment.

Isolates haploid germ cells from the immune system.

Prevents immune attacks on sperm cells.

Maintains an immunosuppressive environment for spermatogenesis.

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34
Q

What are the four key steps of spermatogenesis?

A

Proliferation of spermatogonia (mitosis).
Meiotic divisions of spermatocytes.
Spermiogenesis (maturation of spermatids to spermatozoa).
Spermiation (release of mature spermatozoa into the lumen).

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35
Q

What are the phases of oogenesis?

A

Fetal Life: Oogonia proliferate and begin meiosis, forming primary oocytes.
At Birth: Primary oocytes are arrested in prophase I.
At Puberty: Meiosis resumes during each menstrual cycle, producing secondary oocytes.
Fertilization: Completes meiosis II if fertilization occurs.

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36
Q

What is spermiogenesis?

A

The process of transforming spermatids into mature spermatozoa, involving:

Nuclear condensation.
Acrosome formation.
Tail (flagellum) development.

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37
Q

What is the role of Leydig cells?

A

Leydig cells produce testosterone, which regulates:

Spermatogenesis.
Development of secondary sexual characteristics.

38
Q

What are the clinical causes of male infertility?

A

Low sperm count (<15 million/mL).
Abnormal sperm morphology.
Poor motility.
Genetic defects.
Hormonal imbalances.
Environmental factors (e.g., smoking, pollutants).

39
Q

What is capacitation, and where does it occur?

A

Capacitation is a series of changes enabling sperm to fertilize an egg. It occurs in the female reproductive tract.

40
Q

What are the three periods of sperm maturation in the epididymis?

A

Transport: Sperm are propelled from the testis to the epididymis.
Storage: Sperm are stored in the tail of the epididymis.
Maturation: Sperm acquire motility and fertilization capacity.

41
Q

What are the three main stages of fertilization?

A

Sperm binding to the zona pellucida.
Acrosome reaction to penetrate the egg.
Fusion of sperm and egg membranes.

42
Q

What are the clinical consequences of blood-testis barrier disruption?

A

Immune system attacks sperm antigens.
Possible sterility due to autoimmune responses.

43
Q

What is the difference between spermatogenesis and spermiogenesis?

A

Spermatogenesis: Includes the entire process of producing sperm cells (mitosis, meiosis, and maturation).
Spermiogenesis: Specifically involves the transformation of spermatids into mature spermatozoa.

44
Q

What happens during the “all-or-none” period of teratogen exposure?

A

In the first two weeks, exposure to teratogens either causes embryonic death or has no effect, as the embryo is not yet implanted.

45
Q

What are the hormonal regulators of spermatogenesis?

A

FSH: Stimulates Sertoli cells.
LH: Stimulates Leydig cells to produce testosterone.

46
Q

What are the main postmeiotic changes in sperm morphology during spermiogenesis?

A

Nuclear changes:
Nucleus condenses and reshapes.
Histones are replaced by protamines.
Cytoplasmic changes:
Cytoplasm is eliminated to make the sperm lighter.
Acrosome forms from the Golgi apparatus, containing enzymes for egg penetration.
Motility enhancements:
Tail (flagellum) forms for propulsion.
Mitochondria spiral around the proximal flagellum for energy production.

47
Q

What structures form during spermiogenesis to enhance motility?

A

A tail (flagellum) forms on the opposite side of the centriole, enabling motility.
Mitochondria are arranged spirally in the proximal flagellum to provide energy.

48
Q

What changes occur in the seminiferous tubules during spermiogenesis?

A

Sertoli cells support developing sperm.
Cytoplasmic bridges keep spermatogonia, spermatocytes, and spermatids connected during development.
Mature sperm are released into the lumen during spermiation.

49
Q

How is the seminiferous tubule structured?

A

Basal compartment: Contains spermatogonia.
Adluminal compartment: Contains spermatocytes and spermatids.
Both compartments are separated by tight junctions of Sertoli cells to form the blood-testis barrier.

50
Q

How does sperm motility develop?

A

Motility is acquired in the epididymis through:
Tubulin phosphorylation.
Calcium and cAMP increase.
Biochemical maturation (e.g., glycoprotein coating).

51
Q

What are the structural changes in sperm during epididymal transit?

A

Stabilization of condensed chromatin.
Surface charge alterations in the plasma membrane.
Acquisition of forward motility.

52
Q

What are the major components of semen?

A

Sperm (~10% of semen volume).
Secretions from the prostate gland and seminal vesicles.
Total volume: ~3.5 mL on average.

53
Q

What are the clinical consequences of disrupted sperm structure?

A

Abnormal sperm morphology (e.g., globozoospermia - round head, lack of acrosome) can result in infertility.
Defects in flagellar motility can impair sperm movement.
Head-tail coupling defects may cause sperm decapitation during movement, leading to infertility.

54
Q

What is spermatogonium, and where is it located?

A

Spermatogonia are the undifferentiated germ cells located outside the blood-testis barrier in the basal compartment of the seminiferous tubules. They are the precursor cells for sperm production.

55
Q

Define oogenesis and its stages.

A

Oogenesis is the process of oocyte development and maturation. It includes:

Primordial follicle stage: Housing primary oocytes arrested in the first meiotic division.

Primary follicle stage: Formation of the zona pellucida and communication between oocyte and follicular cells.

Secondary follicle stage: Formation of the theca folliculi and antral spaces.

Tertiary follicle stage: Meiosis resumes before ovulation, leading to the secondary oocyte.

56
Q

What triggers ovulation, and what is the ovulated complex?

A

Ovulation is triggered by a surge in LH (Luteinizing Hormone). The ovulated complex includes:

The oocyte
The zona pellucida
Corona radiata
A sticky matrix of cumulus oophorus cells.

57
Q

Describe the menstrual cycle and its phases.

A

The menstrual cycle consists of two coexisting events:

Ovarian cycle: Folliculogenesis and ovulation.
Uterine cycle: Endometrial preparation for embryo implantation. If fertilization does not occur, the endometrium is shed during menstruation.

58
Q

What is the role of the corpus luteum?

A

The corpus luteum secretes progesterone and estrogens to prepare the endometrium for potential embryo implantation. If fertilization occurs, it remains functional for about 5-6 months. If not, it degenerates into the corpus albicans.

59
Q

Define Mittelschmerz and its cause.

A

Mittelschmerz is a mid-cycle abdominal pain experienced by some women during ovulation. It is caused by slight bleeding into the abdominal cavity and follicle enlargement before rupture.

60
Q

What are the types of ovarian follicles, and how do they differ?

A

Primordial follicles: Contain primary oocytes arrested in prophase I, with squamous granulosa cells.
Primary follicles: Formation of the zona pellucida, cuboidal granulosa cells.
Secondary follicles: Multilayered granulosa cells, theca interna producing androgens.
Antral follicles: Fluid-filled antrum formation, estrogen production.
Graafian follicles: Fully mature and ready for ovulation.

61
Q

How is the oocyte transported after ovulation?

A

The oocyte is captured by the fimbriae and transported through the uterine tube by cilia movement and muscular contractions. It remains in the ampulla for fertilization before moving to the uterus.

62
Q

How many primordial follicles begin folliculogenesis each month?

A

5-12 (up to 50) primordial follicles begin folliculogenesis each month.

63
Q

What maintains the arrest of meiosis I in the diplotene stage in primary follicles?

A

High levels of cAMP from oocyte and follicular cells inhibit maturation-promoting factor (MPF).
cGMP from follicular cells inhibits phosphodiesterase, preventing the breakdown of cAMP.
Oocyte maturation inhibitor (OMI), produced by granulosa cells, also helps maintain arrest.

64
Q

How do follicular cells and oocytes communicate?

A

Through gap junctions and microvilli that penetrate the zona pellucida.

65
Q

When does the menstrual cycle begin and end?

A

Begins with menarche at puberty.
Ends with menopause, approximately 40 years later.

66
Q

What happens to the uterine cycle if fertilization does not occur?

A

The endometrium is shed during menstruation, and a new cycle begins.

67
Q

Where do oocytes and their associated follicles mature in the ovary?

A

In the cortex of the ovary.

68
Q

What is the primary characteristic of primordial follicles?

A

Contain primary oocytes arrested in the first meiotic division.
Surrounded by a squamous layer of granulosa cells that produce AMH (anti-Mullerian hormone).

69
Q

What is OMI?

A

Oocyte maturation inhibitor

A follicular cell protein that reaches the oocyte through gap junctions.

Inhibition of Meiosis: OMI helps maintain the primary oocyte in its arrested state during the diplotene stage of prophase I of meiosis.
cAMP Maintenance: It works by maintaining high levels of cyclic adenosine monophosphate (cAMP) within the oocyte, which inhibits the activation of maturation-promoting factor (MPF).
This inhibition ensures that the oocyte remains arrested until the proper hormonal signals, such as the LH surge, trigger the resumption of meiosis during ovulation.

70
Q

What triggers the resumption of meiosis in response to the LH surge?

A

The resumption of meiosis is triggered by granulosa cells, as the oocyte itself does not possess LH receptors.

71
Q

What happens to gap junctions between cumulus cells and the oocyte in response to the LH surge?

A

Cumulus cells shut down their gap junctions, reducing the transfer of cAMP and cGMP from cumulus cells to the oocyte.

72
Q

How does the reduction of cGMP in the oocyte affect PDE3A?

A

The reduction of cGMP allows the activation of PDE3A (phosphodiesterase 3A).

73
Q

What is the role of PDE3A in the oocyte during meiosis resumption?

A

PDE3A breaks down intraoocytic cAMP into 5′AMP, leading to a decline in cAMP levels.

74
Q

What does the decline in cAMP concentration in the oocyte lead to?

A

The decline in cAMP sets off a signaling pathway that activates MPF (Maturation Promoting Factor), triggering the resumption of meiosis.

75
Q

What is the role of FSH and LH in the growth of secondary follicles?

A

FSH receptors on granulosa cells stimulate the production of estrogens.
LH receptors on theca interna cells stimulate the production of testosterone, which is converted to estrogens by granulosa cells.

76
Q

What marks the transition from preantral to antral follicles?

A

Formation of small fluid-filled spaces (Call-Exner bodies) in preantral follicles.
These spaces coalesce to form the antrum in antral follicles, filled with liquor folliculi rich in hyaluronic acid.

77
Q

How does the dominant follicle become independent of FSH?

A

The dominant follicle secretes inhibin, which reduces FSH levels, allowing it to mature independently while non-dominant follicles degenerate.

78
Q

What occurs during ovulation?

A

LH surge induces inflammatory reactions in the outer follicle.
The follicle ruptures, releasing the oocyte with the zona pellucida, corona radiata, and cumulus oophorus matrix.
The oocyte is captured by the fimbriae and transported through the uterine tube.

79
Q

What happens to the corpus luteum if fertilization occurs?

A

The corpus luteum becomes the gravidic corpus luteum, producing hormones (progesterone and estrogens) for 5-6 months.
After 6 months, the placenta takes over hormone production

80
Q

What happens to the corpus luteum if fertilization does not occur?

A

It becomes the menstrual corpus luteum, ceases hormone production after ~10 days, and regresses into the corpus albicans (scar tissue).

81
Q

What is the role of the fimbriae and uterine tube in egg transport?

A

Fimbriae: Sweep the ovulated egg into the uterine tube.
Uterine tube: Uses cilia and muscular contractions to transport the egg or zygote to the uterus.
Ampulla: Slow transport (~72 hours), where fertilization usually occurs.
Isthmus: Rapid transport (~8 hours) to the uterus.

82
Q

What are some causes of blockage in the uterine tube, and what is the impact?

A

Causes: Infection, inflammation, endometriosis.
Impact: Blockage is a major cause of infertility in women.

83
Q

What changes occur in sperm during capacitation?

A

Removal of cholesterol and glycoproteins from the sperm membrane.

Increase in membrane fluidity and permeability to bicarbonate and calcium.

Activation of signaling pathways, including protein phosphorylation.

Exposure of molecules needed for binding to the zona pellucida.

membrane hyperpolarization

increased intracellular calcium

Removal of sperm plasma membrane proteins.

Reorganization of lipids and proteins.

84
Q

What guides sperm to the egg during fertilization?

A

Chemoattractants released by the oocyte and follicular fluid.
Thermotaxis: Sperm respond to temperature gradients in the uterine tube.
Only capacitated sperm respond to these stimuli.

85
Q

What is the role of Lgr5+ positive stem cells in the ovarian germinative/surface epithelium?

A

Lgr5+ positive stem cells repair the damage caused to the ovarian surface epithelium after each ovulation.

86
Q

What does Lgr5 stand for?

A

Lgr5 stands for Leucine-rich repeat-containing G protein-coupled receptor 5.

87
Q

How is Lgr5+ associated with ovarian cancer?

A

Lgr5+ is associated with very malignant ovarian cancer.

88
Q

How long does it take for the egg to travel from the uterine tube to the uterus after ovulation?

A

The egg typically takes about 3-4 days to travel from the uterine tube to the uterus.

89
Q

When does the proliferative phase occur, and what happens during this phase?

A

The proliferative phase occurs after menstruation (approximately day 6 to day 14 in a 28-day cycle). During this phase, rising estrogen levels stimulate the regrowth of the endometrial lining in preparation for potential embryo implantation.

90
Q

When does the secretory phase of the menstrual cycle begin, and what happens during this phase?

A

The secretory phase begins after ovulation (approximately day 15 to day 28 in a 28-day cycle). During this phase, the corpus luteum secretes progesterone, causing the endometrial lining to thicken and become more glandular, in preparation for embryo implantation.

91
Q

How long do sperm remain viable in the female reproductive tract?

A

Spermatozoa can remain viable in the female reproductive tract for up to 80 hours.

92
Q

What is the process of fertilization once sperm reaches the oocyte?

A

Sperm capacitation allows sperm to bind to the zona pellucida of the oocyte.
The sperm undergoes an acrosome reaction, releasing enzymes that help it penetrate the zona pellucida and fuse with the oocyte membrane.
Upon fusion, the sperm delivers its genetic material, resulting in fertilization and the formation of a zygote.

Embryology (4 decks)

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