RPA pregnancy Flashcards

1
Q

epigastric pain in pre eclampsia

A

night>day
very severe
not relieved by movement and antacids
spontaneously resolve

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2
Q

creatinine in pregnancy

A

normal range up to 60
usually lower in pregnancy
>70 is suspicious

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3
Q

Low platelets in pregnancy

A

accept >100 in pregnancy

but increased incidence in pre-eclampsia

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4
Q

pre-existing hypertension in pregnancy

A

noted before 20 weeks gestation

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5
Q

pre-eclampsia vs chronic hypertension

A

need to see if it resolves post pregnancy

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6
Q

trends of BP during pregnancy

A

high at the start then falls and rises agian

U shape

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7
Q

pathogenesis of pre-eclapsmi

A

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

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8
Q

antiangiogenic factors in preeclampsia

A

SFLT1 and PIGF endoglin (soluble antiangiogenic factors) are elevated in preeclampsia and prior onset

-> endothelial dysfunction

used to predict and diagnose preeclampsia

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9
Q

prevention of pre-eclampsia

A

aspirin of risk >1:100

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10
Q

kidneys preclampsia

A

renal biopsy - glomerloendotheliosis

proteinuria
tubular dysfunction

rising creatining later (>90)

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11
Q

haematological preclampsia

A

DIC
thrombocytopenia
Incr APTT and PI
haemolysis

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12
Q

liver pre-eclampsia

A

ischaemia
haemorrhages
abrnoaml LFTs (but ALP increased in all pregnant women)
epigastric/RUQ pain

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13
Q

CNS pre-eclampsia

A
ischaemia, haemorrhages
haedaches
visual disturbance
retinal vasospasm
hyperreflexia/conus
eclampsia (not all women progress to eclampsia, depends on which vascular bed is affected)
stroke
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14
Q

who is prone to eclampsia

A

young
african

white women less so

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15
Q

seizure prophylaxis in pre-eclampsia

A

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
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16
Q

fetus pre-eclampsia

A

IUGR

see slides

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17
Q

severe pre-eclampsia

A
BP >160/100
symptoms
renal dysfunction
ELLP
hyperreflexia, clonus
18
Q

reflexes in pregnant women

A

increased physiologically

19
Q

management of pre-eclampsia

A

admit

  1. 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)

  1. stabilise fluid status
    - women are usually odematous but intraveously dry
  2. treat coagulopathy, thormbocytopenia
20
Q

prevention of pre-eclampsia

A

low dose aspirin
calcium
only treat thrombophillia in antiphospholipid
see slides

21
Q

recurrence of pre-clampsia

A

30-60%

22
Q

what does pre-eclampsia increase the risk of

A

ESRD x4
chronic hypertension x3.7
IHD 2.1

stroke, PVD, DVT, T2DM, TSH high

23
Q

hyperemesis gravidarum def

A

1st trimester

weight loss and impaired nutrition

24
Q

intrahepatic cholestasis LFTs

A

transamintis

25
Q

Intrahepatic cholestasis treatment

A

ODCA but recent PITCHES trial showed no reduction in itch or neonatal outcomes

26
Q

hyperemesis gravidarum thyroid funciton tests

A

transient hyperthyroxinaemia and suppressed TSH related to cross-reactivity with HCG

27
Q

acute fatty liver of pregnancy

A

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

28
Q

LCHAD in acute fatty liver of pregnancy

A

LCHAD deficiency in fetus

29
Q

intrahepatic cholestasis of pregnancy clinical features

A

pruritis soles and palms

assos w preterm labour, meconium stained amniuotic fluid
bile acid >100 assos w stillbirth

30
Q

what rheumatological conditions may deteriorate during pregnancy

A

everything except RA

31
Q

what antibodies cross the placenta to cause congenital heart block

A

SSA/SSB

32
Q

what antibodies cross the placenta to cause graves

A

thyroid receptor antibody may cause fetal/neonatal thyrotoxicosis but rare

33
Q

what haematological autoimmune condition can have antibodies that cross the placenta to affect the fetus

A

thrombocytopenia (also rare)

34
Q

what neurological autoimmune condition can have antibodies that cross the placenta to affect the fetus

A

myasthenia gravis (20-30% fetus affected)

35
Q

how does APLS affect pregnancy

A

thorugh both thormbotic and non-thrombotic effects

36
Q

how many women have a normal pregnancy in APLS

A

50% normal pregnancy

very few have thrombotic events
most risk on the fetal side

37
Q

treatment of APLS in pregnancy

A

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

38
Q

Altered pharmacokinetics in pregnancy

A

Absorption, protein bindingm hepatic metabolism, renal excretion

protein bound or renally excreted meds need dose increase (e.g. antiepileptics)

39
Q

why do most conditions flare in post partum period

A

switch from Th2 dominant to Th1 dominant immune balance

40
Q

radiation from VQ/CTPA in maternal patient

A

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