RPA pregnancy Flashcards
epigastric pain in pre eclampsia
night>day
very severe
not relieved by movement and antacids
spontaneously resolve
creatinine in pregnancy
normal range up to 60
usually lower in pregnancy
>70 is suspicious
Low platelets in pregnancy
accept >100 in pregnancy
but increased incidence in pre-eclampsia
pre-existing hypertension in pregnancy
noted before 20 weeks gestation
pre-eclampsia vs chronic hypertension
need to see if it resolves post pregnancy
trends of BP during pregnancy
high at the start then falls and rises agian
U shape
pathogenesis of pre-eclapsmi
combination of: genetic factorsm abnormal trophoblastm oxidative stress, angiotensin 1 autoantibodies
the normal spiral arteries that should penetrate into the uterine wall to supply blood and oxygen does not undergo the appropriate changes to do that to the placenta.
the placenta then becomes hypoxic and releases things into the circulation - incluing oxidative stress, proinflammatory cytokines, increased AT autoantibodies and syncytiotrophoblast microparticles and nanoparticles
that causes increased antiangiogenesis (decreased VEGF and PIGF) and affects various organs
antiangiogenic factors in preeclampsia
SFLT1 and PIGF endoglin (soluble antiangiogenic factors) are elevated in preeclampsia and prior onset
-> endothelial dysfunction
used to predict and diagnose preeclampsia
prevention of pre-eclampsia
aspirin of risk >1:100
kidneys preclampsia
renal biopsy - glomerloendotheliosis
proteinuria
tubular dysfunction
rising creatining later (>90)
haematological preclampsia
DIC
thrombocytopenia
Incr APTT and PI
haemolysis
liver pre-eclampsia
ischaemia
haemorrhages
abrnoaml LFTs (but ALP increased in all pregnant women)
epigastric/RUQ pain
CNS pre-eclampsia
ischaemia, haemorrhages haedaches visual disturbance retinal vasospasm hyperreflexia/conus eclampsia (not all women progress to eclampsia, depends on which vascular bed is affected) stroke
who is prone to eclampsia
young
african
white women less so
seizure prophylaxis in pre-eclampsia
lower the BP
sz secondary to hypertensive encephalopathy, ischaemia and oedema
magnesium sulphate works as a cerebral dilator
- can be used as prevention and treatment of eclamptic seizures
- reduce seizures by 50%
- NNT for caucasian population is high
fetus pre-eclampsia
IUGR
see slides
severe pre-eclampsia
BP >160/100 symptoms renal dysfunction ELLP hyperreflexia, clonus
reflexes in pregnant women
increased physiologically
management of pre-eclampsia
admit
- control BP
- alpha methyldopa/clonidine
- labetalol
- nifedipine
- hydralazine
- prazosin
rapid escalation
HTN often refractory
cautious w tiny baby with bad CTG due to ?perfusion abnormality
avoid diuretics (plasmavolume depletion) and ACEI (fetotoxic)
- stabilise fluid status
- women are usually odematous but intraveously dry - treat coagulopathy, thormbocytopenia
prevention of pre-eclampsia
low dose aspirin
calcium
only treat thrombophillia in antiphospholipid
see slides
recurrence of pre-clampsia
30-60%
what does pre-eclampsia increase the risk of
ESRD x4
chronic hypertension x3.7
IHD 2.1
stroke, PVD, DVT, T2DM, TSH high
hyperemesis gravidarum def
1st trimester
weight loss and impaired nutrition
intrahepatic cholestasis LFTs
transamintis
Intrahepatic cholestasis treatment
ODCA but recent PITCHES trial showed no reduction in itch or neonatal outcomes
hyperemesis gravidarum thyroid funciton tests
transient hyperthyroxinaemia and suppressed TSH related to cross-reactivity with HCG
acute fatty liver of pregnancy
very catastrophic
usually t3
microvesciular fatty infiltration (unlike NASH which is macrovescicular)
presents w malaise, A, N, V jaundice impaired level of consciousness features of preeclampsia treatment of delivery of fetus regardless of gestation HYPOGLYCAEMIA
diagnosis clinically w SWANSEA criteria
fetal mortality > maternal mortality
LCHAD in acute fatty liver of pregnancy
LCHAD deficiency in fetus
intrahepatic cholestasis of pregnancy clinical features
pruritis soles and palms
assos w preterm labour, meconium stained amniuotic fluid
bile acid >100 assos w stillbirth
what rheumatological conditions may deteriorate during pregnancy
everything except RA
what antibodies cross the placenta to cause congenital heart block
SSA/SSB
what antibodies cross the placenta to cause graves
thyroid receptor antibody may cause fetal/neonatal thyrotoxicosis but rare
what haematological autoimmune condition can have antibodies that cross the placenta to affect the fetus
thrombocytopenia (also rare)
what neurological autoimmune condition can have antibodies that cross the placenta to affect the fetus
myasthenia gravis (20-30% fetus affected)
how does APLS affect pregnancy
thorugh both thormbotic and non-thrombotic effects
how many women have a normal pregnancy in APLS
50% normal pregnancy
very few have thrombotic events
most risk on the fetal side
treatment of APLS in pregnancy
probably some benefit of heparin in conjucntion w aspirin cf aspirin alone
APL but no thrombosis or fetal loss
- aspirin or nothing
ALP w previous thrombosis
- LMWH and aspirin
Recurrent miscarriages
- aspirin
Fetal loss/severe PET
- prophylactic LMWH + aspirin
?hydroxychloroquine
Altered pharmacokinetics in pregnancy
Absorption, protein bindingm hepatic metabolism, renal excretion
protein bound or renally excreted meds need dose increase (e.g. antiepileptics)
why do most conditions flare in post partum period
switch from Th2 dominant to Th1 dominant immune balance
radiation from VQ/CTPA in maternal patient
same radiation to fetus (very low and insignificant)
CTPA has greater radiation to breasts
but CTPA can diagnose more non PE pathologies
VQ in postpartum women requires them to discard breastmilk
