Lecture 13 Flashcards by Tom Fresen

antenatal care

regular midwife visits 
check SFH plotted on GROW chart
foetal movements discussed 
BP 
urine dipstick for proteinurea 
GTT 
diabetes

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placental dysfunction

small
abnormal
impaired function

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inability to support foetal growth

FGR

pre-eclampsia (PE)

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FGR + PE

increasing foetal demand with gestation leading to a still birth

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FGR

failure to reach genetic growth potential

5-6% of pregnancies

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consequences of FGR

latrogenic preterm birth
neonatal death
life long disabilities

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developmental programming in FGR

obesity
FGR
metabolic syndromes 
diabetes 
schizophrenia

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still births

1:220
age increases risk
smoking
chronic hypertension

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placental abnormalities in FGR

size and structure
functional abnormalities
could be due to incest

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size and structure

placental abnormalities in FGR

villous and vascular tree in placenta

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functional abnormalities

placental abnormalities in FGR

nutrient transport
cell turnover
endocrine function
vascular funciton

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macroscopic placenta

small

infarcts

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microscopic placenta

decreased branching of villous tree 
fewer and smaller terminal villi 
reduced surface area 
thicker SYNC 
slower diffusion

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placental vascularisation

decrease in FGR of placental villi

can effect flow

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increase in placental vascularisation resistance in FGR

placental arteries constrict more

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nutrient transport in FGR

reduced

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placental hormones in FGR

reduced

hPL, PGH, PIGF

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maternal vascular malperfusion

maternal blood delivered to foetus via spiral uterine arteries

high volume blood flow to placenta

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transformation of maternal vascular malperfusion during early pregnancy

EVT - extravillous trophoblast

enlarged sinus
high volume
low resistance blood flow

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PE symptoms

hypertension
proteinurea
oedema

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PE associated with

FGR

multisystem disease

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PE treatment

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delivery

PE characterised by

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higher resistance in maternal arteries

adherent spiral arteries remodelling

uteroplacental function reduced

placental damage due to shear force from high pressure blood flow

oxidative stress

micro-particles activating immune and vascular endothelial

vascular endothelium inappropriately activated

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oedema
vasoconstriction
proteinurea
cerebral artery spasms 
platelet activation 
clumping

factors released by PE placenta

reduces ATP in maternal vascular endothelial

why can you not investigate PE

uterine artery doppler is not abnormal

transcriptonomics and PE

330 PE human placentas microarray bioinformatics mRNA showed common levels

causes of PE according to bioinformatics

immunological canorial maternal chromosome abnormalities

placental screening for second trimester

``` high risk women screened look at serum biomarkers fetal biometry umbilical and uterine artery doppler placental size and morphology ```

doppler looks at

iliac artery via ultrasound

doppler FGR and PE

reduced blood flow (EDF) increased resistance diastolic notching

doppler in maternal vascular malperfusion

reduced oxygen and nutrient supply

placental morphology

size - depth, length, diameter texture cord insertion

fetal biometry and EFW

head circumference abdominal circumference femur length umbilical artery doppler

pre term delivery

single biggest cause of neonatal deaths risk of mortality if inversely proportional to gestation age at birth 75% PPROM, PTL

pre-term delivery causes

unknown | infections

risk factors of pre-term delivery

previous PTB | cervical trauma

prior history of pre-term birth | MEDICAL

prophylactic vaginal progesterone | prophylactic cervical cercalge

prior history of pre-term birth | MECHANICAL

prophylactic vaginal progesterone prophylactic cervical cercalge stitching is required

PTL medication

tocolytics - nifidapiene atosbian indomethacin

tocolytics - nifidapiene

relax uterine muscle | ca2+ channel blocker

atosbian

oxytocin receptor antagonist

indomethacin

COX inhibitor | stops PG synthesis

mouse model advantages

``` ease of genetic manipulation can study KO on foetus and placenta expresses GLUT1, Ca2+ ATPases and system A cheap short gestation both have hemochorial placentas ```

mouse model disadvantages

short gestation different to humans large litters difference in placental structures

placental structures in mice and humans

``` decidua (maternal) invasive trophoblast placenta chorionic plate umbilical cord ```

human difference

villous placenta one main structure hemoMONOchorical invasive trophoblast

mouse differences

labyrinthine 2 main zones hemoTRIchorical invasive trophoblast

available mouse models

placental specific Igf2 KO

PO Igf2 KO

KO in placenta and normal everywhere else FGR and placental growth restriction 50% decrease in labyrinthine surface area

IGF2

key placental growth factor

IGF2 KO

reduced passive permeability | structural abnormalities

IGF2 KO system A

not reduced increases at E16 placenta tries to overcome small foetal size

Lecture 13 Flashcards

(53 cards)