Fertilisation & week 1 development Flashcards

1
Q

Superior

A

above something else towards the head

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2
Q

Cranial

A

towards the head

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3
Q

caudal

A

towards the tail

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4
Q

Vental

A

Towards the front (umbilical cord)

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5
Q

Dorsal

A

Towards the back

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6
Q

Transverse plain

A

Dividing the cranial from the caudal (cutting embryo across waist)

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7
Q

Sagittal section

A

Dividing the embryo into right and left halves

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8
Q

Coronal section

A

dividing the embryo up into ventral and dorsal (taking a slice down the “front” of the embryo)

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9
Q

Two techniques used to date a pregnancy

A

Menstrual age
Fertilisation age

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10
Q

How is Menstrual age used?

A
  • Used by clinicians
    Dates pregnancy from the womens first day of last menstrual period
    Used as:
  • Cheap
  • Fairly reliable
  • Easy to identify
    Three equal trimesters
    1= 1st day of last period-12 weeks
    2= 12 weeks+ 1 day to 28 weeks
    3= week 28+1 to week40
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11
Q

How is fertilisation age used?

A
  • Used by embryologists
    More specific
    Divided into 3 stages
  • Early development (cell division, pre- embryonic)
  • Embryonic (organogenesis) period (E)
  • Foetal period (F)
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12
Q

How common are human birth defects?

A

1 in 44 births in UK

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13
Q

Major causes of congenital malformations

A

Unknown (idiopathic) = 50%
Multifactorial= 25%
Major environmental= 7%
Monogenic= 8%
Chromosomal= 10%

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14
Q

Percentage of birth defects detected prenatal

A

<60%

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15
Q

Genetic & environmental

A
  • Meiosis
  • Mitosis
    EN
  • Teratogens
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16
Q

Genetic causes of birth defects

A

Monogenic
- defective gene on autosome
Chromosomal
- Numerical (aneuploidy)
E.G.
Patau
Edwards
Downs
- Structural
E.G.
Cri du chat
Pallister killian syndrome

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17
Q

Symptoms of genetic causes

A
  • Growth retardation
  • Intellectual impairment
  • Craniofacial development
  • Congenital heart defects
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18
Q

What are teratogens?

A

Environmental influence that is “monster forming”

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19
Q

Examples of Teratogens

A

Infections (TORCH)
Chemicals
Physical
Maternal disease
Deficiency

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20
Q

Sensitivity to teratogens

A

Risk of congenital malformations from teratogens is at the highest when exposed between 3-5 weeks fertilisation
age
Before 3 weeks, no
placenta. So likelihood
of abnormality at this time
is very low as pregnancy
would likely just not survive

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21
Q

What does TORCH stand for?

A

Toxoplasmosis
Other (Hep B, Syphilis)
Rubella (German measles)
Cytomegalovirus (CMV)
Herpes simplex virus (HSV)
each of these diseases cross the placenta and may cause birth defects

22
Q

Toxoplasmosis & congenital malformations

A
  • Paracite
  • Found in cat faeces and undercooked raw meat
  • Usually asymptomatic

Congenital malformations
- Inflammation of retina and eye/ microphthalmia
- Hearing loss
- Enlarged liver spleen
- Hydrocephaly
- Microcephaly

23
Q

Rubella & congenital malformations

A
  • Infection passes over placenta in first 3 months of pregnancy
  • Rates of rubella have decreased since the MMR vaccine

Congenital malformations
- Cloudy cornea
- Intellectual disability
- Microcephaly
- Heart defects

24
Q

Cytomegalovirus (CMV) & congenital malformations

A
  • Virus that crosses the placenta
  • Infection via bodily fluids
  • Usually asymptomatic

Congenital malformations
- Inflammation of retina/ microphthalmia
- Enlarged spleen or liver
- Mineral deposits on the brain
- Microcephaly
- Psychomotor impediments

25
Q

Herpes virus & congenital malformations

A

Herpes simplex
- Varicella zoster virus (chicken pox)
- Most dangerous in between 13-20 weeks or just before birth to two days pp

Congenital malformations
- Segmental skinloss/ scarring
- Limb hypoplasia/ paresis
- Microcephaly
- Visual defects

26
Q

Zika virus & congenital malformations

A
  • Mosquito
  • Bodily fluids (of injected person)
  • Fever, rash, joint pain, red eyes

Congenital malformations
- Microcephaly
- Severe cognitive disabilities

27
Q

Chemical- Thalidomide

A
  • Developed in west germany in 1950s
  • Prescribed for morning sickness
  • Shortened or absent limbs
  • Now used to treat leprosy and HIV
28
Q

Chemical- alcohol

A
  • Clear relationship between alcohol consumption and congenital abnormalities

Associated with:
- Prenatal and postnatal growth retardation
- Intellectual disability
- Impaired motor ability and coordination

Foetal alcohol syndrome
- smell eye openings
- Smooth philtrum
- Thin upper lip

29
Q

Radiation & congenital malformations

A
  • Causes cell death or chromosome changes
  • CNS most sensitive
  • Most sensitive in the first trimester

Congenital malfomations
- Microcephaly
- Mental and cognitive disabilities
- Haemopoietic malignancies and leukemia

30
Q

Maternal disease & congenital malformations

A
  • Can cause cellular structural defects and changes in cellular physiology

Congenital malformations
- Macrosomia
- Ventricular septal defects
- Spina bifida
- Renal agenesis

31
Q

Folic acid deficiency & congenital malformations

A
  • Malformations in CNS
  • OTC supplements reduce risk of malformation by around 60%

Congenital malformations
- Spina bifida
- Anencephaly

32
Q

What are the 4 features of male gametes

A
  • plasma membrane
  • Head (acrosome, nucleus)
  • Middle piece (loaded with mitochondria)
  • Tail (Flagellum)
33
Q

What are the 6 features of female gametes

A
  • Cortical granules
  • Zona pellucida
  • Cell membrane
  • Cytoplasm
  • Pronucleus
  • Corona Radiata
34
Q

Outline of the hormone cycle

A

Referred to as the HPG axis
Begins in the thalamus
Moves to pituitary and travels to the gonads (in the case of bio females, the ovaries)
Acts on gametes to begin maturation

35
Q

What does the hypothalamus screte?

36
Q

What does secretion of GnRH cause?

A

acts on neurones in the anterior pituitary gland and causes the release of gonadotropins:
- Follicle stimulating hormone (FSH)
- Luteinising hormone (LH)

37
Q

Formation of primary follicle

A

Local androgens act on the primordial follicle (diploid) to encourage development into a primary follicle (2n).

38
Q

Primary follicle to late secondary follicle

A

Primary follicle develops into an early secondary follicle through addition of ++FSH and +LH from the anterior pituitary. FSH + LH + Cholesterol + Androgens = Oestrogen

Steps repeated for ESF to form LSF

39
Q

Late secondary follicle to graafian follicle

A

Late Secondary follicle begins creating pools of follicular fluid, stimulated by FSH and LH, oestrogen is produced, late secondary follicle divides producing a polar body and a secondary oocyte (n) enclosed in the graafian follicle

Pools of follicular fluid coalesce and form an antrum in graafian follicle

40
Q

What does oestrogen do to HPG axis?

A

decrease FSH and LH output until threshold oestrogen is met

41
Q

What happens when threshold oestrogen is met?

A

graafian follicle releases Inhibin B, which decreases production of FSH and Oestrogen feeds positively on anterior pituitary to secrete huge surge of LH.

42
Q

What does LH do to vessels?

A

acts on vessels local to graafian follicle to become leaky and as a result, the antrum swells
LH activates proteases anchoring secondary oocyte within graafian follicle

43
Q

What happens to the secondary oocyte within the graafian follicle?

A

Pressure and lack of anchor cause eruption of secondary oocyte out of graafian follicle- OVULATION

44
Q

What happens to the remainder of the graafian follicle

A

LH transforms it into corpus luteum, produces progesterone & oestrogen for 10 days. If no fertilisation of secondary oocyte, corpus luteum degrades and pro & oestro drop.

45
Q

What happens if fertilisation occurs?

A

syncytiotrophoblasts of blastocyst secrete hCG which signals corpus luteum to maintain oestrogen and progesterone secretion to support the pregnancy until a placenta can take over.

46
Q

Overview of fertilisation

A
  • Fusion of male & female gametes to form zygote
  • Capacitation of sperm
  • Acrosome reaction
  • Formation of zygote
  • Fusion of pronuclei
47
Q

Where does fertilisation usually occur?

A
  • Ampulla of the uterine tube
  • Fimbriae sweep oocyte (Egg) into the uterine tube
  • Sperm undergo capacitation in female reproductive tract
48
Q

What is a zygote?

A

oocyte + sperm

49
Q

What happens to capacitated sperm?

A
  • Pass through corona radiate
  • Acrosome releases enzymes that allow sperm to penetrate zona pellucida
  • Sperm penetration initiates cortical reaction (prevents any more sperm entering oocyte- now zygote)
  • Zona pellucida becomes impenetrable= zone reaction
50
Q

What happens on days 1-3 post fertilisation

A

0= fertilisation day
every 24 hours zygote divides by cleavage= doubles number of cells (blastomeres)

51
Q

Formation of morula

A

Day 4
16-32 cells
Inner cell mass= embryo proper (embryoblasts)
Outer cell mass= placenta (trophoblasts)

52
Q

Formation of Blastocyst

A

Formation of fluid filled cavity by day 5
Separates cells into a:
- Compact mass (embryoblasts)
- Thinner outer layer (trophoblasts)
Zona Pelludica jacket breaks away (shed) as teh blastocyst makes its way into the body of the uterus allowing the uterine attachment