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Physiology > Embryology > Flashcards

Embryology Flashcards

1
Q

What are the changes which occur to the genetic material of the egg/sperm following fertilisation?

A
  1. Sperm entry causes oocyte completion of meiosis II (extrusion of second polar body)
  2. Paternal pronucleus unwinds and enlarges
  3. Syngamy (following centralisation of pronuclei) occurs
  4. Metaphase plate established
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2
Q

What are the structural changes which occur during the first few cell divisions following fertilisation?

A

No growth; just division of totipotent cells:
- Increases nuclear to cytoplasmic ratio
- Restricted by zona pellucida

Compaction (creation of inner and outer cells):
- Morula forms (cluster of cells)
- Polarisation of embryo occurs (not all totipotent)
- Outer cells have E-cadherin (defines epithelium)

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3
Q

What is the blastocyst? How does the blastocyst form?

A

Blastocyst/coel = fluid filled cavity
- Created by tight junctions of outer cells causing ion gradient (Na+)
- Draws water in
- Trophectoderm becomes placental trophoblast
- Inner cell mass becomes embryo proper and placental mesoderm

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4
Q

Describe the stages of development from fertilisation to an early stage embryo:

A
  1. Fertilisation (syngamy) occurs
  2. Initial cleavage divisions
  3. Compaction (morula formation)
  4. Blastocyst formation
  5. Inner cell mass development
  6. Placental and embryo proper formation
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5
Q

How does the early embryo get to the uterus for implantation?

A

Regulation of ciliary beating (most significant):
- Stimulated to beat towards egg to help sperm (due to oestradiol)
- Then to beat towards uterus (due to progesterone)
- Blastocyst travels with cumulus cells

Other movement due to:
- Smooth muscle contractions
- Flow of tubular secretions

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6
Q

What are the different molecular markers found on the inner cell mass and trophectoderm? How do they arise?

A

Trophectoderm: Cdx2, Gata3, Eomes (Elf5 expressed)

Inner cell mass (ICM): Nanog; Gata6; Oct4 (Elf5 not-expressed as DNA methylated)

Occurs due to:
- Maternal gradients of mRNA (bicoid/dorsal etc..)
- Zygotic genome activation allows cells to respond based on their position
- Cell fate due to specific gene expression
- Sperm influence: pronucleus/pericentriolar matter and small non-coding RNAs

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7
Q

What are some mechanisms of epigenetic control on DNA? (5 examples)

A
  • DNA methylation (turn gene “off”): E.g. Elf5 methylated in ICm but not trophectoderm
  • Histone modification
  • Non-coding RNAs
  • Chromatin remodelers
  • High order chromatin structures
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8
Q

How might the difference between a mule (male donkey; female horse) and a hinny (male horse; female donkey) be explained?

A

Unequal contribution of DNA methylation from sperm and egg

Imprinted genes:
- Silence gene copy depends on parent of origin (paternal IGF2 is always expressed)

X-inactivation (dosage compensation):
- Non-coding RNAs expressed by one X
- Causes other X to condense and silence its gene expression = Barr body formed

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9
Q

Why is implantation necessary? How is it achieved (general principle)?

A

Blastocyst needs to implant as it cannot self-sustain its growth (requires uterus)

Achieved through:
- Molecular and hormonal cross-talk between uterus and blastocyst
- Must both be morphologically and molecularly ready for implantation

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10
Q

What is diapause? How can it be achieved?

A

Prevention of blastocyst implantation until uterus is receptive:
- Coordinated with ovarian cycle
- Prolactin controlled to halt corpus luteum formation
- Increases survival chance by timing birth

Species dependent so can be achieved by:
- Facultative delayed implantation (behavioural): few days delay; implantation induced by suckling = mice/marsupials
- Obligatory diapause (environmental): week/month to coordinate with correct day length (deer)

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11
Q

What are the hormonal signals which allow implantation? How has this been shown experimentally?

A

Implantation requires both oestrogen and progesterone:
- Progesterone dominance with superimposed oestrogen window
- Oestrogen makes luminal cells responsive to blastocyst signals

Shown by:
- Ovariectomised rats (after pregnancy) given exogenous hormones allows implantation
- Oestrogen bump detected just before implantation

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12
Q

What are the changes which occur to the uterus to prepare for successful implantation?

A

Structural changes:
- Microvilli shorten
- Pinopodes activate (uterine walls move closer together)
- Endometrial glands form

Chemical Changes:
- Mucin expression decreases: mucin has negative change which would repel embryo
- Expression of epidermal growth factors (EGFs) and heparin binding (EGF-like) GF
- Leukaemia inhibitory factor (LIF) promotes endometrial receptivity (attracts blastocyst)

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13
Q

What is the decidualisation reaction and when does it occur?

A

Morphological and functional changes around the area of implantation (ONLY for invasive implantation!):
- Oestrogen ➡LIF ➡prostaglandin around implantation site
- Attracts leukocytes to area
- Increases vasculature surrounding (dilatation)
- Uterine stroma differentiates into decidua to provide lipids/glycogen as part of placenta

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14
Q

What chemical and morphological changes occur to the blastocyst to implant?

A

Hatching from zona pellucida:
- LIF produced by uterus induces strypsin
- Strypsin in a proteolytic enzyme to hatch

Binding molecules:
- Integrins (E.g ErbB) and cadherins on blastocyst expression induced by oesteopontin
- Bind HB-EGF on uterus

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15
Q

Why are pinopodes important? What is the evidence for their importance?

A

Determines the level of uterine fluids:
- Significant for multiple foetuses

Infertility caused by exogenous fluid injection

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16
Q

What are the different types of implantation?

A

Invasive implantation:
- Conceptus breaks through epithelium invading stroma (forms decidua)
- Embryo develops in uterine wall
- Uterine NK cells prevent blastocyst going too far
- Humans, cats, dogs, mice… (Mice have crypts to encourage implantation at particular points

Non-invasive implantation:
- Epithelium of endometrium maintained and becomes incorporated into placenta
- Blastocyst is larger (with more extraembryonic tissue) on implantation
- No decidualisation
- Pigs, sheep, cows, horses

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17
Q

What are the different mechanisms by which the corpus luteum is maintained in different species? Give species examples. (5 ways)

A
  • Long-ovarian cycle: length = gestational period so no special changes needed (dogs)
  • Neuro-endocrine link: act of mating causes hypothalamus stimulation (GnRH produced) causing ovulation (cats) or CL maintenance (mice)
  • Luteotrophic factor secretion: Hcg produced by embryo to increase maternal progesterone (humans)
  • Inhibition of luteolytic factors: E.g. pig embryo produces oestrogen to inhibit PGF2α
  • Formation of accessory CL: pregnant horses secrete PMSG to stimulate second ovulation which then produces progesterone
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18
Q

How is maternal recognition of pregnancy achieved?

A

Maintenance of corpus luteum:
- Produces progesterone

Placental progesterone production:
- CL needed until placenta forms

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19
Q

What is a placenta? What are the functions of it and its attached tissues?

A

Close apposition of umbilical and uterine bloodstreams across the chorion for purposes of physiological exchange.

Functions:
- Supply of nutrients
- Supply of oxygen
- Immunological protection
- Protection from trauma (or teratogens)
- Hormone secretion (IFN-τ, hCG, steroids) E.g. insulin antagonising hormones
- Removal of waste

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20
Q

What are the extraembryonic structures during development? E.g. humans, fish

A

Surrounding layers:
- Shell and shell membranes (if applicable)
- Chorion (trophoblast cells)
- Aminon

Amnion houses:
- Yolk sac (nutrient rich)
- Embryo
- Allantois (facilitates gas exchange and absorption of waste products)

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21
Q

What are the different strategies by which embryos gain nutrients (give animal examples):

A
  • Placentotrophy (absorption across foetal membrane): can be either haemotrophic (direct transfer between bloodstreams) or histiotrophic (uterine secretion absorption)
  • Lecithotrophy: foetus gains nutrients from yolk sac and O2 from surrounding water/air
  • Epitheliopathy: embryos eat specialised uterine wall (alpine salamander)
  • Oophagy: eat unfertile eggs (great white shark)
  • Embryophagy: eat sibling (fire salamander)
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22
Q

Why is progesterone important in the maintenance of pregnancy?

A

In establishing pregnancy/early embryo:
- Maintains uterine milk secretion until placenta forms

Controlling maternal physiology:
- Increases GFR to allow for increased waste excretion
- Insulin antagonising effect (diabetogenic)

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23
Q

How does the placenta exchange nutrients? Give specific examples.

A

(Placenta uses up to 1/3rd of nutrients from mother itself)

Simple diffusion:
- O2 diffuses freely
- Ions, fatty acids, cholesterol
- Soluble N waste (urea) and CO2

Facilitated diffusion:
- Huge transporter capacity (never rate limiting)
- Lactate and glucose

Active transport:
- Potentially toxic molecules (Cu, Ca, Pi) out
- Na+ flux is 1000x foetal need (used to transport other molecules

Receptor mediated endo/pino/phagocytosis:
- Fe2+
- IgGs

24
Q

What adaptations allow the foetus to get enough oxygen?

A

O2 diffuses freely and reaches equilibrium given adaptations of foetal Hb:
- Increased [Hb] and of higher affinity
- Less sensitive to DPG
- More to Haldane effect (pH)

25
Q

How do placental structures protect from physical and chemical trauma? Give an example of an iatrogenic threat.

A

Physical protection:
- Foetal membranes and amniotic fluid.

Chemical protection:
- From teratogens (external influences which induce developmental abnormalities)
- Iatrogenic (thalidomide, griseofulvin, chemotherapies)
- Non-iatrogenic (LSD, cocaine, ethanol, plants, environmental pollutants)

Griseofulvin: used to treat fungal infections
- Interfere with developmental processes
- Damage foetal DNA

26
Q

How does the placenta protect from immunological rejection? Why are complex strategies necessary?

A

Complexity necessary to avoid pathogenic mimicry/exploitation. E.g. MHC I expression not switched off completely.

Strategies:
- Foetal trophoblast cells downregulate MHC I expression (can be upregulated again)
- Expression of non-classical MHC I (E.g. HLA-G which is universal in population = not-foreign recognised)
- Modulation of maternal immune system
- Physical barrier to immune cells

27
Q

How does the foetus regulate the maternal immune system?

A

Local:
- Uterine milk proteins (HLA-G) suppress lymphocyte proliferation in ruminant

Systemically:
- Human foetus suppresses T cell proliferation
- Upregulates oestrogen production
- Th1to Th2 shift induced (downregulated cell mediated but compensate by upregulated antibodies)

28
Q

What are the major overarching changes which occur to maternal physiology during pregnancy?

A
  • Hormonal changes
  • Mechanical changes to support weight gain and physical space required for foetus
  • Increase in cardiac output
  • Increase in waste removal capacity
  • Respiratory changes
  • Metabolic changes
29
Q

Detail the hormonal changes necessary to the mother during pregnancy.

A

Progesterone “pro-pregnancy; anti-birth”:
- Either from CL throughout pregnancy or taken over by placenta

Oestrogen “anti-pregnancy; pro-birth” (though relatively high levels during pregnancy too):
- These average levels may not reflect local concentration ([Oestrogen] high and [progesterone] low in mare overall but not locally in placenta)

Almost all hormones change: thyroid; adrenal glands; PTH; IGFs; prolactin

30
Q

Detail the mechanical changes to the body, vasculature and urinary system necessary for maternal physiology to support pregnancy:

A

Increase in CO to maintain BP:
- Stroke volume increased (heart chambers dilate)
- Increased cardiac wall thickness
- TPR decreases (vasodilation due to oestrogen)

Heart physiologically moved up due to foetus:
- Displaces QRS axis on ECG

Urinary system:
- GFR massively increased )due to progesterone)
- Relaxin/NO vasodilates afferent+efferent arterioles
- Reduces urea/creatine seen

31
Q

Detail the respiratory changes necessary to the mother during pregnancy.

A

O2 demand increases 20% but vital capacity decreases due to pressure – mechanisms to counter needed

Increase tidal volume:
Minute volume = rate x tidal volume
- Airway and ribcage dilatation
- Central respiratory drive
- Breathing rate increases

32
Q

Detail the metabolic changes necessary to the mother during pregnancy.

A
  • Storage of nutrient to prepare for lactation
  • Diabetes mimicking state (insulin antagonising hormones): β-cell proliferation to keep up with increased glucose in blood
  • Gastrointestinal/liver hypertrophy of cells
  • Ca2+ mobilisation (activation of Vit D and increased kidney reabsorption)
  • Thyroid hormone increase (iodine needed): oestrogens increase thyroid binding globulins. Hcg can mimic TSH (pseudo-hyperthyroid state)
  • Morning sickness due to FGF-15
33
Q

How might physiological anaemia occur during pregnancy? How does maternal physiology compensate?

A

Erythropoiesis cannot keep pace with blood volume increase
- [Platelets] decreases so compensated for by increased clotting factors (mother hypercoagulable post birth)
- Vasodilation and subsequent baroreceptor activation pulls fluid in (dilates [platelets])
- After birth placenta/uterus acts as transfusion bank

34
Q

How could you measure foetal growth? (5 ways)

A
  • Size measurement (femur/head circumference)
  • Direct post-mortem
  • Weight (post-birth)
  • Placental growth (not accurate)
  • Ultrasound
35
Q

What are the influences on foetal growth?

A
  • Genetic (ethnicity/genetic imperfections (E.g. osteogenesis imperfecta = smaller)/imprinted genes)
  • Endocrine
  • Maternal influences (capacity/nutrition/disease/parity/socioeconomics)
  • Placental condition (surface area can be increased by proliferation of placental villi/vascular innervation increase)
36
Q

What is the evidence for a correlation between parity and nutritional state of the mother for foetal birthweight?

A

Parity = comparison of lambs to same mother throughout life:
- 2nd lamb largest
- Then decreases with age

Nutritional state:
- Foetuses show ‘catch-up growth’ if short time low nutrition ends
- Dutch hunger: if mothers’ in third trimester then catch-up growth not possible so babies smaller

37
Q

What effects does cortisol have on the foetus to prepare for birth?

A

Due to release of ACTH:
- Starts surfactant production in lungs
- Induces stem cell budding from aortic endothelium in aorta-gonad-mesonephros (AGM) region to allow for haematopoiesis (mainly by spleen and liver not bone marrow)
- PNMT enzyme formation in adrenal medulla (adrenaline can be made)
- Upregulate β-adrenergic receptors in lung epithelium so lungs can respond
- Metanephric kidney formation with increase Na/K ATPase action and increased GFR
- Gut maturation
- Metabolic maturation to allow for storage (gluconeogenic enzyme production) and activation of deiodinase (convert T4 to T3)

38
Q

How does foetal metabolism change in preparation for birth?

A

Fundamental change from catabolic (energy demanding) to anabolic (energy storing) AND continuous to intermittent energy gain.

  • Lipids/amino acids start to be used alongside glucose
  • Liver transitions from haematopoietic to metabolic organ
  • Gut maturation (structure; mobility; enzymes)
  • Pancreas develops (α/δ/β cells)
39
Q

How do foetal kidneys change in preparation for birth?

A

Go from fluid environment (fluid homeostasis not an issue) to air

AND must develop ability to remove waste (without needing umbilical cord)

Changes:
- Kidney blood supply increases 10-fold from foetus to adult
- Become able to produce hypertonic urine (only hypotonic as foetus produced)

40
Q

How does foetal heart and vasculature change from foetus to neonate?

A

Foetus:
- Heart working at top end of range (fewer myofibrils and restricted by fluid filled lungs)
- Parallel arrangement between placenta and heart (due to forman ovale and pulmonary to aorta)
- Separated laminar flow to keep blood from mixing fully

Neonate:
- Triggered by decrease in pulmonary resistance
- FO closes then seals
- Haematopoiesis starts after first few weeks

41
Q

How does foetal blood composition differ from adult?

A

Foetus induces net gas transfer from mother (left shifted)

  • Haemoglobin has higher oxygen affinity (ααββ tetramer in adult vs ααγγ in foetus)
  • Haemoglobin not DPG inhibited
  • Higher haemoglobin concentration
  • Haldane shift results in further left shift in foetal haemoglobin (but right in mother) = increases difference across placenta (more O2 gain)
42
Q

How do the adrenal glands partake in positive feedback to prepare the foetus for birth?

A
  • Foetal ACTH induces cortisol release
  • Cortisol allows for PNMT enzyme to form
  • Allows adrenaline production
  • Adrenaline stimulates hypothalamic-pituitary-adrenal axis to produce more ACTH
43
Q

How do lungs change from foetus to neonate?

A

Fluid to air= huge difference

Reduce compliance:
- Elastin production
- Surfactant production

Muscle required for breathing:
- Practice ‘breaths’ of amnion induce maturation
- Shown by cutting phrenic nerve which inhibits maturation

Reversal of fluid secreting to fluid expulsing organ:
- Change direction of ion pumping (controlled by adrenaline after birth)

44
Q

What are the main substances/conditions responsible for inducing birth?

A

Decrease in P/O ratio:
- Progesterone decline (reduction in hyperpolarising myometrium and inhibiting gap junction formation)
- Oestrogen increase (Prepares for coordinated myometrial activity
- Prostaglandins (locally) - E.g. PGF2α induces luteolysis of CL allowing uterine contractions
- Oxytocin

45
Q

How does the shift from progesterone to oestrogen dominance allow for birth?

A

Progesterone decrease:
- Releases inhibition of myometrial gap junction formation
- Reduces hyperpolarisation
- Releases inhibition of oxytocin receptor insertion (OTR)
- Releases inhibition of PG synthesis

Oestrogen increase:
- Due to progesterone to oestrogen converting enzymes
- Prepares for coordinated myometrial activity (more gap junction proteins and Ca2+ channels) = easier for APs to propagate
- Increases trophoblast PGF2α secretion
- Increases PG uterine receptors
Increases oxytocin receptors (late pregnancy)

46
Q

What structural changes occur in the uterus to prepare for birth?

A

Oestrogen = rapid ripening:
- Reduced fibrous organisation and crosslinking
- More elastin
- More hyaluronic acid and lubricant
- Some species use CL to secrete relaxin (induces relaxation and repair after birth)

47
Q

How does the foetus signal that it is ready for birth?

A

Cortisol must be high:
- Shown by veratrum californium poisoning in sheep (where foetal axis damaged)
- Infusion of cortisol/ACTH/CRH induces birth
- Foetal brain maturation allows cortisol release

Effects of cortisol:
- Changes trophoblast steroidogenic enzyme expression to lower P/O

For polytocous births (many):
- May delay to allow all to be ready by regressing CLs secreting relaxin

48
Q

What is the ferguson reflex?

A

Positive feedback loop:
- Contraction causes pressure on cervix
- Pressure releases oxytocin
- Oxytocin increases contractions

49
Q

Describe the composition of milk:

A

Lactose:
- Production of α-lactalbumin alters galactosyl transferase specificity to produce lactose from glucose and UDP-galactose
- Collects in Golgi (water drawn in by osmosis) then solution exocytosed

Protein:
- Colloidal suspension created
- Caseins (phosphoproteins) produced ( E.g. calcium caseinate micelles with -ve charge
- Whey proteins (dissolved albumins and globulins)

Lipids (emulsion of fat globules):
- Bilayer surface charge prevents coalescence
- Various C14-18 fatty acids; small size rise more slowly (less buoyant)

Ions: isotonic despite high ion and lactose (prevents infant dehydration)
- High K+; low Na+ (tight junctions prevent plasma to milk paracellular flux)
- Active transport of Ca2+, PO43-, Mg2+, vitamins
- Iron in milk low – infants compensate due to hepatic stores

50
Q

What are foetal adaptations to allow for lactation?

A

Digestive adaptations:
- Gastric rennin including chyosin to coagulate casein to curds and whey
- Lactase production

Responsive to milk fractions:
- First is more watery (stop dehydration)
- Second is higher in lipids (energy)

51
Q

How are lactogenesis and galactopoiesis stimulated?

A

Lactogenesis:
- Alveolar epithelial cells develop capacity to store milk as pregnancy continues
- Due to drop in placental lactogens and progesterone

Galactopoiesis (maintenance of lactation):
- Local autocrine route: suckling frequency controls pressure of atrophy and inhibitory protein levels
- Neuroendocrine PRL reflex: suckling = reduced dopamin = more prolactin
- Endocrine regulation: GH (predominance in ruminant); PRL (predominates in other)
- Other hormones synergistic (T3, oestrogen , progesterone, glucocorticoids

51
Q

What maternal changes are necessary to prepare for lactation?

A

Very metabolically expensive - eat lots!

Prolactin:
- Inhibited by hypothalamic dopamine (weird)
- Causes growth: duct development and enhanced adipose tissue
- Metabolic changes - anti-insulin
- Maternal behaviour
- Suppression of ovarian cycle
- Hello from daddit

52
Q

What stimulates the onset of breathing? What is the evidence for this?

A

Triggered by:
- Asphyxiation (hypoxia)
- Temperature change
- Mechanosensory change to air

Evidence:
- Blind or deaf babies have same response
- Water birth delays this

53
Q

How does a foetus have high hypoxic tolerance?

A

Adaptive mechanisms due to low O2 environment in utero:
- Like high altitude adaptation
- Foetal haemoglobin (with DPG resistance)
- High RBC concentration
- Glycogen reserves in cardiac muscle

Short-term adaptation (e.g. like diving mammal):
- Hypoxia induced suppression of thermogenesis and reduced heart rate
- Shunting blood from periphery to heart and brain
- High breathing rate (larger dead space in lungs)

54
Q

Why do neonates struggle with thermogenesis?

A

Several mechanisms unavailable:
- Little hair
- Voluntary muscles too weak for continued shivering

Use:
- Peripheral vasoconstriction to maintain abdominal temperature
- BAT stimulated (by hypothalamic NA production): rich in mitochondria with uncoupling protein (UCP1)
- Release of FFAs to BAT tissue
- BAT releases lipoprotein lipase (LPL) to stimulate fatty acid uptake
- T3 produced (metabolic stimulation) creating a +ve feedback loop as T3 stimulates UCP1 expression

Physiology (8 decks)

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