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Women's Health > Fetal Development/growth and the Placenta > Flashcards

Fetal Development/growth and the Placenta Flashcards

1
Q

Describe the structure of the placenta and how substances are moved between the mother and the fetus

A

Maternal spiral arteries and veins
-substances diffuse from the villi basal plate =(intervillous space)=> chorionic villi

1 umbilical vein => fetus => 2 umbilical arteries

Blood does not mix

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2
Q

Describe the structure of the early spiral arteries

What are the 2 methods of substance transfer

A

Initally histitrophic
-spiral arteries blocked by trophoblastic plug

Becomes haemotrophic
-plug removed, mouth expands to accommodate more blood

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3
Q

Describe how

  • CO2
  • Glucose
  • FA
  • AA is trasnported
A

CO2
-diffuses across syncytiotrophoblast, CA buffered

Glucose
-GLUT1 across STB

FA

  • LPL breaks down TAG in LP => FA
  • transported to FATP bound to FABP

AA

  • NaAAcotransport, nonessential, essential AA exchange
  • Na, Cl cotranport
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4
Q

How is fluid homeostasis maintained in the fetus

A

Maintained by placenta, fetal membrane

  • kidneys provide dilute urine (immature ADH)
  • bladder fills and empties every 20-30mins
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5
Q

What is found in the amniotic fluid

How is amniotic fluid homeostasis maintained

A 
Urine
Amniotic membrane secretions
Fetal lung secretions
Saliva
Fetal and amniotic cells

Fetus swallows fluid from wk12 onwards

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6
Q

How doe the GI system develop in the fetus
-digestive enzymes, when are they found from
-digestive hormones, where and when are they found from
When is it formed by

A

Formed by wk19

Digestive enzymes
-present by wk9, mature at term

Gastrin motilin, somatostatin

  • regulate growth and dev
  • gut synthesised, mature by wk24
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7
Q

Describe how glucose homeostasis is maintained

  • where does glucose come from
  • how is it used
  • where does the insulin come from
A

Dependent on placental transfer

  • glycogen storage in fetal liver
  • not capable of gluconeogenesis

Fetal insulin and IGF

  • lipogenesis
  • anabolic, anticatabolic effects for growth
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8
Q

Describe the physiological control of the fetal heart

A

HR affected by ANS control (PNS dominated)

  • NA/A
  • chemo/baroceptors
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9
Q

Describe the circulatory route of blood from the placenta

Describe the fetal haemoglobin and its characteristics

A

Placenta => 1 umbilical vein => ductus venosus (bypass liver) => foramen ovale (bypass pulmonary circulatotion) => ductus arteriosus (bypass lungs) => 2 umbilical arteries

HbF

  • increased O2 affinity, [HbF]
  • decreased PO2

HbA
-increases from wk28

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10
Q

Describe the fetal hypoxic response

A 
Decreased HR
Decreased cerebral resistance
Increased umbilical artery resistance
Increased flow to heart, adrenals
Decreased flow to kidneys => oligohydramnios
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11
Q

Describe the cells in the lungs and their functions

A

T2 alveolar cells secrete surfactant from wk24 => decrease alveolar surface tension
-PL, C, protein

T1 alveolar cells

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12
Q

What is neonatal resp distress
What is the pathophysiology
How would you manage this

A

Not enough surfactant

Decreased compliance, alveolar collapse
Increased work to breathe

Exogenous surfactant
-synthetic/modified natural
Cortisol
-stimulate lung dev and surfactant prod

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13
Q 
How does
-umbilical clamping
-inspiration
-secretions
change at delivery
A

Umbilical clamping
-decreased RA pressure, FO closes

Inspiration

  • VD of pulmonary arteries => decreased R
  • decreased F via FO, DA

Secretions

  • lung secretions decrease
  • surfactant increases
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14
Q

How is placental transfer used in the production of fetal and maternal hormones

A

Maternal cholesterol
Converted to pregnenolone
-fetus converts this into DHA, DHAS
-can be converted into types of estrogen for maternal use

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15
Q

What are the 3 stages of embryo growth

-what are the main characteristics

A 
Stage 1 (4-20wk)
-hyperplasia, rapid mitosis, increase in DNA

Stage 2 (21-28)

  • hyperplasia and hypertrophy
  • declining mitosis but cell size increases
  • greatest weight gain here

Stage 3 (29-40)

  • hypertrophy
  • rapid increase in cell size
  • accumulate fat, muscle, connective tissue
  • greatest variation in weight here
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16
Q

What is appropriate for gestational age

A

Following the expected trends in weight as gestational age increases

17
Q

What is fetal growth restriction

  • what are the short term consequences
  • what are the long term consequences
A 
Growth doesn't follow expected trend
Pathological restriction/IUGR
-stillbirth
-seizures
-ICU admission
-hypothermia, hypoglycaemia

Long term impact

  • CHD, HT
  • T2D, strokes
18
Q

What does it mean to be small for gestational age

  • what are the 2 main types
  • management
A

<3-10th cent
Following trends in weight but below estimations consistently

Symmetrical SGA - prolonged poor growth from early pregnancy

  • healthy, normal
  • chromosomal, congenital issues
  • alcohol, cigarettes, drugs
  • TORCHZS
  • malnutrition

Assess for pathological cause, infections
Monitor growth frequently

Asymmetrical - placenta fails to provide adequate nutrition late in pregnancy

  • placental insufficiency, PET
  • alcohol, cigarettes, drugs
  • congenital, chromosomal

Assess for absent end diastolic flow in umbilical circulation with Doppler
Monitor growth frequently
Consider early delivery

19
Q

How would you detect, prevent and manage SGA

A

Detection and prevention

  • decreased PAPPA, high uterine flow resistance (poor placental function)
  • aspirin, monitor growth, decrease PET risk

Management

  • if FGR=> early delivery with steroids
  • if SGA=> induce before term
20
Q

How would you interpret a fetal doppler for the

  • umbilical artery
  • MCA
A

Fetal doppler, judge direction and quality of blood flow
-generates pulsatility index

Umbilical artery

  • if line falls under x axis => flow reversed
  • if line falls on x axis => no flow at that point
  • if pulsatility index increases, blood has to work harder to be moved around

MCA

  • if diastole is higher than expected => MCA being prioritised for some reason
  • if PI decreases => be worried
21
Q

What are the possible growth outcomes for twins

  • what birth would be low risk
  • what births would be high risk
A

Both grow normally
Both SGA
AGA, FGR => may need to deliver at different times

Low risk
-DC

High risk

  • MC
  • potential selective IUGR
  • potential twin to twin transfusion
22
Q

What does it mean to be large for gestational age
-what are the causes
-what are the risks
How would you manage this

A

> 90th centile
Healthy large => large parents

Poorly controlled maternal diabetes

  • shoulder dystocia (fat accumulates on shoulders)
  • hypoglycaemia (exposed to increased glucose, produces extra insulin
  • increased chance of maternal complications
    • PPH
    • Caesarean may be needed
23
Q

What are the consequences of shoulder dystocia

A

Brachial plexus injury
-Erbs palsy

Fractured humerus, clavicle
-Asphyxia, death

24
Q

When is the earliest that you can detect a fetal heartbeat?

A

6-7wks

CRL 1-2mm

Women's Health (29 decks)

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