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Human Repro > Lecture 13 > Flashcards

Lecture 13 Flashcards

1
Q

antenatal care

A 
regular midwife visits 
check SFH plotted on GROW chart
foetal movements discussed 
BP 
urine dipstick for proteinurea 
GTT 
diabetes
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2
Q

placental dysfunction

A

small
abnormal
impaired function

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3
Q

inability to support foetal growth

A

FGR

pre-eclampsia (PE)

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4
Q

FGR + PE

A

increasing foetal demand with gestation leading to a still birth

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5
Q

FGR

A

failure to reach genetic growth potential

5-6% of pregnancies

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6
Q

consequences of FGR

A

latrogenic preterm birth
neonatal death
life long disabilities

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7
Q

developmental programming in FGR

A 
obesity
FGR
metabolic syndromes 
diabetes 
schizophrenia
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8
Q

still births

A

1:220
age increases risk
smoking
chronic hypertension

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9
Q

placental abnormalities in FGR

A

size and structure
functional abnormalities
could be due to incest

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10
Q

size and structure

placental abnormalities in FGR

A

villous and vascular tree in placenta

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11
Q

functional abnormalities

placental abnormalities in FGR

A

nutrient transport
cell turnover
endocrine function
vascular funciton

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12
Q

macroscopic placenta

A

small

infarcts

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13
Q

microscopic placenta

A 
decreased branching of villous tree 
fewer and smaller terminal villi 
reduced surface area 
thicker SYNC 
slower diffusion
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14
Q

placental vascularisation

A

decrease in FGR of placental villi

can effect flow

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15
Q

increase in placental vascularisation resistance in FGR

A

placental arteries constrict more

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16
Q

nutrient transport in FGR

A

reduced

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17
Q

placental hormones in FGR

A

reduced

hPL, PGH, PIGF

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18
Q

maternal vascular malperfusion

A

maternal blood delivered to foetus via spiral uterine arteries

high volume blood flow to placenta

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19
Q

transformation of maternal vascular malperfusion during early pregnancy

A

EVT - extravillous trophoblast

enlarged sinus
high volume
low resistance blood flow

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20
Q

PE symptoms

A

hypertension
proteinurea
oedema

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21
Q

PE associated with

A

FGR

multisystem disease

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22
Q

PE treatment

A

delivery

23
Q

PE characterised by

A

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

24
Q

vascular endothelium inappropriately activated

A 
oedema
vasoconstriction
proteinurea
cerebral artery spasms 
platelet activation 
clumping
25
Q

factors released by PE placenta

A

reduces ATP in maternal vascular endothelial

26
Q

why can you not investigate PE

A

uterine artery doppler is not abnormal

27
Q

transcriptonomics and PE

A

330 PE human placentas
microarray
bioinformatics
mRNA showed common levels

28
Q

causes of PE according to bioinformatics

A

immunological
canorial
maternal
chromosome abnormalities

29
Q

placental screening for second trimester

A 
high risk women screened 
look at serum biomarkers 
fetal biometry
umbilical and uterine artery doppler 
placental size and morphology
30
Q

doppler looks at

A

iliac artery via ultrasound

31
Q

doppler FGR and PE

A

reduced blood flow (EDF)
increased resistance
diastolic notching

32
Q

doppler in maternal vascular malperfusion

A

reduced oxygen and nutrient supply

33
Q

placental morphology

A

size - depth, length, diameter
texture
cord insertion

34
Q

fetal biometry and EFW

A

head circumference
abdominal circumference
femur length
umbilical artery doppler

35
Q

pre term delivery

A

single biggest cause of neonatal deaths

risk of mortality if inversely proportional to gestation age at birth

75% PPROM, PTL

36
Q

pre-term delivery causes

A

unknown

infections

37
Q

risk factors of pre-term delivery

A

previous PTB

cervical trauma

38
Q

prior history of pre-term birth

MEDICAL

A

prophylactic vaginal progesterone

prophylactic cervical cercalge

39
Q

prior history of pre-term birth

MECHANICAL

A

prophylactic vaginal progesterone
prophylactic cervical cercalge
stitching is required

40
Q

PTL medication

A

tocolytics - nifidapiene
atosbian
indomethacin

41
Q

tocolytics - nifidapiene

A

relax uterine muscle

ca2+ channel blocker

42
Q

atosbian

A

oxytocin receptor antagonist

43
Q

indomethacin

A

COX inhibitor

stops PG synthesis

44
Q

mouse model advantages

A 
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
45
Q

mouse model disadvantages

A

short gestation
different to humans
large litters
difference in placental structures

46
Q

placental structures in mice and humans

A 
decidua (maternal)
invasive trophoblast 
placenta 
chorionic plate 
umbilical cord
47
Q

human difference

A

villous placenta
one main structure
hemoMONOchorical
invasive trophoblast

48
Q

mouse differences

A

labyrinthine
2 main zones
hemoTRIchorical
invasive trophoblast

49
Q

available mouse models

A

placental specific Igf2 KO

50
Q

PO Igf2 KO

A

KO in placenta and normal everywhere else

FGR and placental growth restriction

50% decrease in labyrinthine surface area

51
Q

IGF2

A

key placental growth factor

52
Q

IGF2 KO

A

reduced passive permeability

structural abnormalities

53
Q

IGF2 KO system A

A

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

Human Repro (11 decks)

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