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Reproductive system > Lecture 18- Foetal physiology > Flashcards

Lecture 18- Foetal physiology Flashcards

1
Q

function of the placenta

A

It supports the developing foetus, in utero, by supplying nutrients, eliminating waste products of the foetus and enabling gas exchange via the maternal blood supply.

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2
Q

The development of the placenta begins during

A

implantation of the blastocyst.

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3
Q

outline the structure of a blastocyst

A
  • 32-64 cells
  • contains two distinct differentiated embryonic cell types:
    • the outer trophoblast cells and the inner cell mass.
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4
Q

The trophoblast cells form

A

the placenta.

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5
Q

The inner cell mass forms

A

the foetus and foetal membranes.

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6
Q

What day does implanation occur and where does it occur?

A
  • Day 6 after it has hatched from zona pellucida
  • Usually implants on superior body of uterus but can implant lower down or on previous C-section scars that are not viable or not in the uterus
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7
Q

What are some problems with invasion of the conceptus into the endometrial wall?

A
  • Too deep: placenta accreta
  • Incomplete invasion: miscarriage or placental insufficiency that can lead to preeclampsia
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8
Q

When does the placenta develop and how?

A
  • Week 2 before anything else
  • From fetal membranes
  • Chorionic sac and amniotic sac separate but then as the amniotic sac enlarges it displaces the chorion and fuses with the chorionic membrane
  • Projections around all surfaces of this membrane concentrated into a small disc like space that becomes the placenta
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9
Q

what does implantation achieve?

A
  • Basic unit of exchange
  • Anchor the placenta
  • Establish maternal blood flow
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10
Q

What are chorionic villi?

A
  • Villi that sprout from the chorion membrane
  • Inner connective tissue core, where fetal vessels can form, and outer layer of syncytiotrophoblasts
  • Maternal blood vessels surround villi so exchange can occur but mixing of circulations never
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11
Q

How do the chorionic villi change over pregnancy?

A

1st trimester: barrier between maternal and fetal blood vessels thick. Full layers of cytotrophoblasts and syncytiotrophoblasts

3rd trimester: barrier less, becomes one layer of trophoblast by reducing cytotrophoblasts

Margination of fetal capillaries and loss of trophoblasts

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12
Q

How is the degree of invasion of the conceptus controlled?

A

the decidua becomes specilaised through decidualisation

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13
Q

Decidualization

A

is a process that results in significant changes to cells of the endometrium in preparation for, and during, pregnancy.

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14
Q

what complications will occur if implantation is correct but decidual reaction is suboptimal

A

complications like miscarriage, infertility or placental insufficiency leading to pre-eclampsia

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15
Q

what complications will occur if implanation is in inocorrect place

A

no decidual reaction so ectopic

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16
Q

Label the gross morphology of the placenta.

A
  • Amnion on outside with chorion vessels underneath
  • Need to check placenta for cotyledons to check none of them have fallen out and can cause post partum haemorraghe
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17
Q
A
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18
Q

oxygenated blood is carried to the foetus via the

A

umbilical vein

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19
Q

deoxygenated blood is carried awya from the fetus via the

A

umbilical arteries

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20
Q

gas exchange at the palcenta

A
  • requires
    • a diffusion barrier- gets thinner as pregnancy progresses
    • a gradient of partial pressure
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21
Q

how is a gradient of partial pressures between the foetus and mother ensured

A

maternal pO2 only icnreases marginally, therefore to make the gradient work the fetal pO2 must be lower than maternal pO2

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22
Q

approx fetal pO2

A

4kPa compared to normal adult 11-13kPa

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23
Q

factors increasing fetal O2 content

A
  • Fetal haemoglobin variant HbF
  • Fetal haematocrit is increased over that in the adult
  • increased maternal production of 2,3 DPG
  • double bohr effect
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24
Q
  • Increased maternal production of 2,3 DPG secondary to
A

Secondary to physiological respiratory alkalosis of pregnancy

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25
Q

fetal Hb

A
  • Predominant form from week 12- term is HbF
  • 2 alpha subunits plus 2 gamma subunits
26
Q

why does HbF have a greater affinity for oxygen than HbA

A

Greater affinity for oxygen because it doesn’t bind 2,3-DPG as effectively as HbA

27
Q

double bohr effect

A
  • Speeds up the process of O2 transfer
  • As CO2 passes into intervillous blood pH decreases
    • Bohr effect
      • Decreasing affinity of Hb for O2
  • At the same time, as CO2 is lost (to the maternal side), pH rises
    • Bohr effect
      • Increasing affinity of Hb for O2
28
Q

CO2 transfer

A
  • Maternal physiological adaption to pregnancy
  • Progesterone driven hyperventilation
    • More CO2 blown off
  • Hence lower pCO2 in maternal blood
  • Concentration gradient created
    • More CO2 will come from foetus to mother more efficiently- to be removed by physiological hyperventilation
29
Q

double haldane effect

A
  • as Hb gives up oxygen it can except more CO2
  • As O2 accepted by foetus from mother, CO2 accepted by mother from foetus
30
Q

difference between double bohr and double haldane effect

A

Bohr

The Bohr effect describes the shift of the hemoglobin dissociation curve to the right by hydrogen ions, which reduces the affinity of hemoglobin for oxygen.

Since the Bohr effect occurs on both sides of oxygen delivery/uptake, it has been called the double Bohr effect.

Haldane

The Haldane effect describes the increased ability of deoxygenated blood to carry more carbon dioxide.

Likewise, the double Haldane effect describes maternal and fetal changes in carbon dioxide and oxygen uptake. The fetal hemoglobin becomes oxygenated and releases carbon dioxide, which has increased binding to the maternal hemoglobin that has just deoxygenated.

31
Q

What are the main blood vessels exchanging the placenta and how are they arranged?

A
  • Endometrial arteries bathe the villi
  • Paired umbilical arteries carry waste products to villi
  • Single umbilical vein takes oxygen and nutrients to fetus
32
Q

oxygenated blood delivered to the foetus via the umbilical vein goes straight to the

A
  • the right side of the heart, bypasses the lungs and gets pumped out of the aorta to the body, which then via the umbilical artery is returned to the mother to be oxygenated
33
Q

The fetal circulatory shunts

A
  • Oxygenated blood from the mother enters the foetus via the umbilical vein
  • By-passes the liver via the ductus venosus
    • Very metabolic organ and would use up oxygen and nutrients
  • Enters Inferior vena cava (IVC) and goes into the right atrium
    • Protect the lung by by-passing the right ventricle and lungs via the foramen ovale and enters the left atrium where blood is bumped out of the heart via the aorta
  • Oxygenated blood can then supply the body and be returned to the placenta for re-oxygenation
34
Q

Ductus venosus

A
  • DV connects umbilical vein carrying oxygenated blood to the IVC
  • Blood enter the right atrium
  • By ensuring shunting of blood around the liver, blood oxygenation saturation is maintained- drops from 70% to 65%
35
Q

Foramen ovale

A
  • Right atrial pressure is greater than in the left atrium
  • Forces leaves (of the valve) of FO apart and blood flows into the LA
  • Septum secundum forms a crest- crista dividends
    o Small ridge on the free border of the septum secundum creates two streams of blood flow
    o Majority flows to the LA
    o Minor proportion flows to the right ventricle, mixing it with blood from SVC (deoxygenated) allows muscle developement
36
Q

Left atrium

*

A
  • Small amount of pulmonary venous return à blood supply to developing lungs
    • Deoxygenated
  • Blood reaches left atrium is mixed therefore saturation is approx. 60%
  • Pumped by LV to aorta
  • Heart and brain get the biggest share of oxygen
37
Q

Ductus arteriosus

A
  • Shunts blood from RV and PT to aorta
  • Joins aorta distal to the supply to the head and heart
38
Q

Fetal response to hypoxia

A
  • Adaptations to manage transient decrease in oxygenation
  • HbF and increased [Hb]
  • Redistribution of flow to protect supply to heart and brain (reducing supply to GIT, kidneys and limbs
  • Fetal heart rate slows in response to hypoxia to reduce O2 demand
  • Fetal chemoreceptor’s detecting decreased pO2 or increased pCO2
    • Vagal stimulation leading to bradycardia
    • Cf adult where vagal inhibition leads to tachycardia
  • Chronic hypoxaemia
    • Growth restriction
    • Behaviour changes
      • Impact on development
39
Q

What is the endocrine function of the placenta?

A
  • hCG from syncytiotrophoblasts maintain corpus luteum in first trimester. urine and blood tests
  • Steroid hormones made to take over corpus luteum and produce enough oestrogen and progesterone to keep body in pregnant state
40
Q

Why may someone have high levels of hCG in their blood?

A
  • Pregnancy specific, from syncytiotrophoblasts
  • Molar pregnancy
  • Testicular cancer
  • Choriocarcinoma
41
Q

How do placenta hormones change the metabolic state of the mother?

A
  • Progesterone: increases appetite to allow increased fat deposition to support fetus and breast feeding
  • Human Placental Lactogen (hCS): creates diabetogenetic state by causing insulin resistance to mother so more glucose availability for fetus
42
Q

How does transport across the placenta occur?

A
  • Simple diffusion: water, gases, electrolytes
  • Facilitated diffusion: glucose
  • Active transport: aa’s, Fe, vitamins
  • Receptor mediated endocytosis: IgG’s
43
Q

How does gas exchange occurs across the placenta?

A
  • Simple diffusion
  • Flow limited and fetal O2 stores are low so adequate flow essential
  • Can have fetal distress (hypoxia) in labour contractions as they compress uteroplacental circulation
44
Q

How does the mother confer immunity?

A
  • IgG antibodies from mother can pass across placenta via receptor mediated endocytosis
  • Protects baby
45
Q

When do teratogens cause the greatest effect in pregnancy?

A
  • Preembryonic: fatal
  • Embryonic (3-6 weeks): sensitive as body systems developing
  • Fetal (9-36 weeks): +/- sensitive apart from CNS
46
Q

What are some harmful substances to the fetus?

A
  • Thalidomide
  • Alcohol (FAS and ARND)
  • Therapeutic drugs (antiepileptic, warfarin, ACEi)
  • Smoking (low birth weight)
  • Drugs (dependency)
47
Q

What are some dangerous infections to have in pregnancy and why?

A

some viruses

Mother is in immunocompromised state so infections more serious, need to check mother’s immunisation status. Poor pregnancy outcomes

48
Q

Hormones necessary for fetal growth

  • *
A
  • Insulin
  • IGFI and IGFII
  • IGF II nutrient independent, dominant in first trimester
  • IGF1 nutrient dependent, dominates in T2 and T3
  • Leptin
    • Placental production
    • Plus EG, TGF-a
49
Q

foetal malnutrition can cause

A
  • can cause symmetrical (whole foetus) or asymmetrical (certain parts of foetus) growth restriction
  • Nutritional and hormonal status during fetal life can influence health in later life
50
Q

dominant cellular growth mechanism from early to late pregnancy

A

hyperplasia –> hypertrophy

51
Q

Amniocentesis

A
  • Sampling of amniotic fluid
  • Allows for collection of fetal cells
  • Useful for diagnostic test e.g. fetal karyotyping
52
Q

production of amniotic fluid

A

Amniotic fluid is essentially composed of fetal urine. This production of urine starts to happen at around 9 weeks.

53
Q

function of amniotic fluid

A
  • protection
  • development of the lungs
54
Q

volume of amniotic fluid

A
  • 10ml at 8weeks
  • Approx 1 litre at 38 weeks
  • Falls away post- expected delivery date
55
Q

Recycling of amniotic fluid

A

One way of recycling the amniotic fluid is by inhaling amniotic fluid by the fetus ‘practicing’ breathing movements. This helps with production of the lung, particularly surfactant.

Another key mechanism for recycling amniotic fluid is by the fetus swallowing the fluid, and so it enters the fetal GI tract. Debris from the GI tract accumulate as meconium, which is passed after delivery as the baby’s first stool.

56
Q

urine production by

A

9 weeks

up to 800 ml a day in T3

57
Q

minor contributors to amniotic fluid

A
  • Minor contributors: lungs and GI tract, placenta and fetal membranes (intramembranous pathway)
58
Q

Composition of amniotic fluid

A

It is mainly composed of water, and electrolytes and substances that that you might typically expect in the urine. There are also elements of the fetal skin that have been lost over the pregnancy.

  • Debris accumulates in the gut
    • Meconium–> debris from am amniotic fluid plus intestinal secretions including bile
    • Green
59
Q
A
60
Q

what is meconium

A
  • debris from am amniotic fluid plus intestinal secretions including bile
  • Green
61
Q

Bilirubin metabolism in the foetus

A
  • During gestation clearance of fetal bilirubin is handled efficiently by the placenta
  • Foetus cannot conjugate bilirubin
    • Immaturity of the liver and intestinal processes for metabolism, conjugation and excretion
  • Physiological jaundice is common

Reproductive system (28 decks)

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