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Obstetrics > problems in pregnancy > Flashcards

problems in pregnancy Flashcards

1
Q

how are UTIs treated in pregnancy?

A

avoid nitrofurantoin in last trimester

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2
Q

what is pre-eclampsia?

A

multisystem disorder characterised by new onset HTN and proteinuria that occurs in second half of pregnancy and resolves with delivery.

one of many hypertensive disorders of pregnancy

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3
Q

what is the normal pattern of blood pressure seen during pregnancy?

A

Normally BP drops in T1 and T2 due to progesterone and reduced vascular resistance. It then slowly rises back to normal in T3. with delivery there is a drop in BP which gradually rises over 4 days.

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4
Q

what is the pathophysiology behind pre-eclampsia ?

A

Thought to be due to abnormal blood flow through the uteroplacental circulation due to inadequate placentation.
normally trophoblasts invade the myometrium and spiral arteries and result in breakdown of the tunica muscularis such that spiral arteries cannot contract. this results in reduced resistance and increased flow.

in pre-eclampsia there is insufficient remodelling of the spiral arteries. Therefore there is high resistance and low flow. The increased BP and low perfusion of the uteroplacental circulation results in systemic inflammatory response and endothelial cell dysfunction.

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5
Q

what are the moderate and high risk factors to pre-eclampsia?

A

moderate:
- nulliparous, multiple pregnancy, >10 yrs between pregnancies, BMI >35, age >40, FHx of pre-eclampsia

severe:
- chronic HTN, pre-eclampsia/ HTN in previous pregnancy, diabetes, chronic kidney disease, SLE/antiphospholipid

others: thrombophilia, hydrops fetalis, triploidy, hydatidiform mole

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6
Q

what are the 3 clinical criteria that must be met for pre-eclampsia?

A
  1. systolic BP
    • > 140 systolic or >90 diastolic on 2 separate occasions (>4 hours apart)
      - OR >160 systolic or >110 diastolic on one occasion
  2. proteinuria:
    • significant proteinuria >300mg in a 24 hour urine sample
    • OR >30mg/UM protein: creatinine ratio
  3. > 20 weeks gestation
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7
Q

what are the symptoms that occur with pre-eclampsia?

A

headache
visual disturbance - blurring, double, flashing lights
epigastric pain/ RUQ - due to hepaticcapsule enlargement/ infarction
vomiting
sudden onset non dependant oedema
hyperreflexia
confusion

may be asymptomatic - which is why BP and urine checked at every appointment.

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8
Q

what is a poor prognostic factor for pre-eclampsia?

A

onset of pre-eclampsia before 34 weeks

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9
Q

how is pre-eclampsia categorised into mild, moderate and severe ?

A

mild: BP 140-149/90-99
moderate: BP 150-179/100-109
severe: BP > 160/110 + proteinuria >0.5g/day
or >140/90 + proteinuria + symptoms

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10
Q

what are the fetal complications of pre-eclampsia?

A

intrauterine growth restriction
intrauterine fetal death

placental abruption, placental infarct

risk of cerebral palsy
risk of prematurity

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11
Q

list some differentials for pre-eclampsia?

A

pregnancy induced HTN - HTN without proteinuria >20 weeks

essential HTN - HTN <20 weeks gestation

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12
Q

what investigations should be carried out to assess pre-eclampsia?

A

BP recording - sitting down (use korakoff sound V for diastolic (usually IV)
24 hour proteinuria recorded or dipstick - if >300mg or +1 or more on dipstick.

FBC - low platelets and low Hb 
U+Es - raised creatinine, urea and lower urine output. 
LFTs - elevated (AST and ALT) in HELLP
INR 
Group and save
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13
Q

what is HELLP syndrome?

A

haemolysis
elevated liver enzymes
low platelets

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14
Q

what is classed as eclampsia?

A

seizures due to pre-eclampsia during pregnancy, labour or within 7 days of birth.

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15
Q

what prophylaxis is can be given to those at risk of pre-eclampsia? who is chosen for this prophylaxis?

A

aspirin 75mg
those with 1 high risk factor or 2 moderate risk factors
given from 12 weeks onwards

any type of HTN in pregnancy will require aspirin in next pregnancy too

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16
Q

how is pre-eclampsia treated?

A

monitoring: regularly check BP, proteinuria, fetal grown scan and CTG - how often depends on severity of pre-eclampsia

treating HTN to reduce risk of cerebral haemorrhage:
1st line = labetolol
2nd line = nifedipine
3rd line = methyl dopa

preventing complications:

  • VTE = LMWH and fluids
  • seizures = MgSO4
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17
Q

what are the side effects of:

a) labetolol
b) nifedipine?
c) methyldopa?

A

labetolol - postural hypotension, fatigue, headaches, N+V, epigastric pain

nifedipine - peripheral oedema, dizziness, flushing, headaches, constipation

methyldopa - drowsiness, headaches, oedema, GI disturbances, dry mouth, postural hypotension, bradycardia and hepatotoxicity

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18
Q

can ACEi be used for HTN in pregnancy?

A

no contraindication - cause congenital abnormalities

also avoid diuretics

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19
Q

what is the only definitive cure for pre eclampsia?

A

delivery of baby
the pregnancy only benefits the baby - therefore weight up the risks and benefits.
if delivered <34 weeks give steroids.

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20
Q

when should a patient with pre-eclampsia be admitted ?

A

if BP >160/110

OR >150/100 + proteinuria

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21
Q

when should a patient with pre-eclampsia be admitted ?

A

if BP >160/110
OR >150/100 + proteinuria

admit for 4 hourly obs

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22
Q

what drugs are used for emergency BP control in pregnancy?

A

hydralazine
labetolol
nifedipine

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23
Q

what post natal care is required in pre-eclampsia?

A

monitor mother for atleast 24 hours post delivery - still at risk of eclampsia
monitor BP regularly for first 2 days and then atleast once a day till day 5
then the need for anti-HTN treatment can be reassessed
warn mum of risk of pre-eclampsia in next pregnancy + need to take aspirin

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24
Q

what is pregnancy induced HTN

A

HTN post 20 weeks but no significant proteinuria

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25
Q

how is pregnancy induced HTN managed?

A

same as pre-eclampsia

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26
Q

who is essential hypertension more common in?

A

older women

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27
Q

is prognosis of essential HTN good or bad?

A

good

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28
Q

what are the risks of having essential HTN?

A

placental abruption

interuterine fetal growth restriction

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29
Q

how is essential HTN treated?

A

same as pre-eclampsia

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30
Q

how is gestational diabetes defined?

A

onset of any degree of glucose intolerance during pregnancy (first recognition in pregnancy)

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31
Q

what’s the pathophysiology behind gestational diabetes?

A

placenta makes anti-insulin hormones to ensure adequate glucose for fetus
maternal pancreas fights this and makes more insulin
in gestational diabetes there is pancreatic exhaustion and anti-insulin hormones win and thus hyperglycaemic state.

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32
Q

list the risk factors of gestational diabetes?

A 
BMI >35
previous gestational diabetes
first degree relative with diabetes
previous macrosomic baby (>4.5kg)
Asian 
PCOS
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33
Q

list the clinical features of gestational diabetes

A

often asymptomatic if pancreatic reserve is just ok

but can present with polydipsia, polyuria and fatigue

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34
Q

what are the fetal complications of gestational diabetes?

A

maternal glucose is high and thus fetal glucose is high and thus fetal pancreas produces lots of insulin resulting in hyperglycaemia and hyperinsulinemia

insulin is a growth hormone:

  • macrosomia - shoulder dystocia, prolonged labour, instrumental delivery, brachial plexus injury
  • organomegaly - especially heart - cardiomegaly
  • erythropoiesis - polycythaemia
  • polyhydramnios
  • hypoglycaemic (high insulin but no glucose once delivered - thus need to ensure regular feeds and IV dextrose)
  • insulin decreases pulmonary phospholipids and thus fetal surfactant and thus can get transient tachypnoea of newborn
  • increased rates of pre-term
  • congenital malformation
  • fetal distress during labour
  • jaundice
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35
Q

what investigations are carried out for gestational diabetes?

A

oral glucose tolerance test

  1. measure fasting plasma glucose
  2. drink 75g glucose drink
  3. measure plasma glucose 2 hours later

diagnosis if:

  • fasting >5.6
  • 2 hours later >7.8mM
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36
Q

when is the oral glucose tolerance test offered to pregnant women?

A

at booking if previous gestational diabetes
at 24-28 weeks if risk factors
at any point if glycosuria +2 or +1 or 2 occasions

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37
Q

how is gestational diabetes managed?

A

life style management
BMs 4x daily
drugs:
- metformin is good in pregnancy and breastfeeding
- glibenclamide - if metformin not tolerated
- insulin in some people

consultant led care
growth scans need to be more regular - 28, 32 and 36 weeks (for accelerating growth or polyhydramnios)

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38
Q

when is insulin offered for gestational diabetes?

A

if fasting glucose >7mM when first tested
or if any of following develop:
- pre meal glucose level >6mM
- post meal glucose >7.5 mM
- fetal abdominal circumference >95th centile

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39
Q

when is delivery planned in a mother with gestational diabetes?

A

37-38 weeks if on treatment

before 40+2 weeks if diet controlled

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40
Q

what post natal care is offered for those with gestational diabetes?

A

stop medications immediately after delivery
check blood glucose before discharge
check fasting glucose around 6-13 weeks and then annually because at increased risk of developing diabetes.

in subsequent pregnancies - OGTT at booking at 24-28 weeks

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41
Q

how is anaemia in pregnancy defined?

A

<110g/L in T1 or less than 105g/L in T2/3 or <100g/L postpartum

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42
Q

what is the pathophysiology behind anaemia developing during pregnancy?

A

there is a dilutional effect - fluid retention (although RBC increase, fluid increases more)
more iron requirements by placenta and fetus leading to iron deficiency (also blood loss)

other factors: haemaglobinopathy, B12/ folate deficiency and haemorrhage

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43
Q

what are the risk factors for developing anaemia during pregnancy?

A 
maternal age
poor diet
low socioeconomic class 
haemoglobinopathy - sickle cell / thalassemia 
anaemia during previous pregnancy
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44
Q

what are the clinical features of anaemia during pregnancy?

A

tired, dyspnoea, dizzy
asymptomatic
pallor on examination and maybe koilonychia

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45
Q

what are the differential diagnosis for microcytic anaemia during pregnancy?

A

iron deficiency
thalassemia
sideroblastic

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46
Q

what are the differential diagnosis for normocytic anaemia during pregnancy?

A

anaemia of chronic disease
marrow infiltration
haemolytic anaemia
CKD

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47
Q

what are the differential diagnosis for macrocytic anaemia during pregnancy?

A 
Folate deficiency 
alcohol 
thyroid - hypothyroid 
Reticulocytosis  
B12 deficiency
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48
Q

what are the complications of iron deficiency anaemia during pregnancy?

A

IUGF
fetal death
prematurity
maternal fatigue and infection

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49
Q

what investigations/screening should be done for anaemia in pregnancy?

A

FBC - all women screened at booking and 28 weeks
(also between 20 and 28 weeks if multiple fetus)

screened for haemoglobinopathy
serum folate - can be used to distinguish types

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50
Q

how is iron deficiency anaemia during pregnancy managed?

A

iron supplements - ferrous sulphate tablets - first line
recheck FBC after 2 weeks
if poor absorption/ resistance can offer parenteral iron infusion (ferinject)

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51
Q

how is folate deficiency managed in pregnancy?

A

folate supplements are taken in first 3 months of pregnancy anyway
if deficiency the mother can take more.

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52
Q

How is B thalassemia managed in pregnancy?

A

folate supplements and blood transfusions as required

aim for >80g/L during pregnancy and >100g/L by delivery

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53
Q

how is sickle cell managed in pregnancy?

A

folate and iron supplements

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54
Q

what is the pathophysiology behind anti-phospholipid syndrome in pregnancy?

A

autoimmune condition and production of auto Ab to phospholipid binding proteins
in vivo results in procoagulation (in vitro anticoag effect)
effects:
- interferes with trophoblast function and differentiation and thus placental efficiency
- activation of complement pathways at maternal-fetal interface
- thrombosis of uteroplacental vasculature (late pregnancy)

can occur in isolation or alongside SLE, systemic sclerosis or RA

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55
Q

what are the clinical features of anti-phospholipid syndrome in pregnancy?

A 
vascular thrombosis:
  - arterial - MI, stroke
  - venous - DVT, P.E
  - microvascular 
recurrent fetal loss - any gestational age
CKD - due to microemboli 
pre-eclampsia 
IUGR
valvular heart problems - mitral / aortic regurg
thrombocytopenia 
livedo reticularis
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56
Q

what is catastrophic anti-phospholipid syndrome?

A

rare life threatening complication whereby multiple microemboli develop causing ischaemia to multiple organs
can be triggered by infection, trauma or surgery
50% mortality

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57
Q

what are the differentials to antiphospholipid syndrome?

A

protein C/S deficiency

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58
Q

what are the investigations that can be done in someone you suspect has anti-phospholipid syndrome? who is investigated?

A

if presents with symptoms - check for DVT with USS

checking Ab titres - anticardiolipin, lupus anticoagulation, anti B2 glycoprotein I

lupus anticoagulant test - test to detect lupus anticoagulant in blood which is associated with pro-thrombotic state.

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59
Q

what auto-Ab are found in anti-phospholipid syndrome?

A

anti cardiolipin - binds cardiolipin
lupus anticoagulation - is a lupus Ab that is prothrombotic
anti B2 glycoprotein I - binds B2 glycoprotein I

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60
Q

what is the diagnostic criteria for anti-phospholipid syndrome?

A

need one clinical criteria and one lab:
clinical criteria:
- vascular thrombosis
- recurrent miscarriage (3 or more)
- premature birth dur to eclampsia or severe pre-eclampsia
- one or more unexplained fetal deaths of normal fetus >10 weeks gestation

lab:
- lupus anticoagulation test - positive test on 2 or more occasions 12 weeks apart
- anti-cardiolipin Ab - medium or high titres on 2 separate occasions >12 weeks apart
- anti B2 glycoprotein I present in serum/ plasma on 2 or more occasions atleast 12 weeks apart

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61
Q

how is antiphospholipid syndrome managed?

A

LMWH - clexane
all women should be considered for thromboprophylaxis in immediate post natal period

future treatment depends on how they presented:

  • recurrent fetal loss - aspirin and LMWH in subsequent pregnancies
  • pre-eclampsia or IUGR previously - aspirin 75mg in subsequent pregnancy
  • vascular thrombosis - life long anticoagulation with warfarin (INR 2-3) and LMWH in subsequent preg
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62
Q

why is pregnancy a risk factor for VTE?

A

procoaguable state because fibrinogen increased and protein S reduced
the changes become more pronounced as pregnancy commences and thus highest risk is in immediate post partum period

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63
Q

what should be done if a DVT is suspected during pregnancy?

A

FBC, UEs, LFTs, clotting
compression USS duplex

don’t do D dimer as this increases in pregnancy anyway

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64
Q

what are the risk factors for VTE in pregnancy?

A

pre-existing risk factors: BMI >30, age>35, thrombophilia, paraplegia, parity >3, medical comorbidities, smoking, varicose veins

obstetric: pre-eclampsia, multiple pregnancy, C section, still birth, prolonge labour, preterm birth, PPH
transient: dehydration, infection, immobility , surgery, ovarian hyperstimulation syndrome

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65
Q

where are the majority of DVTs and why

A

left side - 90%

left iliac vein can become compressed between iliac artery and ovarian artery

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66
Q

what investigations should be done if a P.E is suspected in pregnancy?

A

ECG, ABG if sats are low
V/Q scan or CTPA

if USS shows DVT need to scan lungs

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67
Q

how is VTE managed in pregnancy? what advice should be given to mum?

A

LMWH - clexane - started immediately and continued throughout pregnancy and 6-12 weeks post partum.
however tell mum to stop dose 24 hours before any planned induction/ C section or if she thinks she is going into labour

(warfarin is contraindicated)
alternatives are unfractionated heparin or oral anticoagulants

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68
Q

what are the risks of V/Q scan and CTPA and which is more risky?

A

V/Q scan - risk of fetal malignancy and breast cancer. but risk of the VTE is much higher

CTPA also carries some risk but safer than V/Q scan

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69
Q

what happens with treatment if the VTE occurs at term?

A

unfractionated heparin should be considered and stopped 6 hours before planned labour/ C section

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70
Q

when is VTE prophylaxis used?

A

all women are assessed for risk factors

if 4 or more risk factors - start LMWH in T1/2 and continue throughout
if 3 - start in T3 (28 weeks onwards)
if 2 - post partum LMWH

any thromboprophylaxis should be contined to 6 weeks post partum

if previous VTE (provoked) - LMWH from 28 weeks
if unprovoked VTE - LMWH throughout
known antithrombin deficiency or antiphospholipid - high dose LMWH throughout

10 day course of LMWH should be considered in all women after C section especially if it was an emergency

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71
Q

when should thromboprophylaxis be discontinued post partum?

A

6 weeks post partum

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72
Q

what type of virus is cytomegalovirus?

A

from the herpes family

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73
Q

what is the most common virus transmitted to fetus during pregnancy?

A

CMV

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74
Q

when does CMV have highest risk to fetus?

A

first trimester

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75
Q

what are clinical features of CMV infection in mother and fetus?

A

in mother can be asymptomatic or flu like symptoms
can also develop mononucleosis (like EBV) - fever, splenomegaly and impaired liver function.

fetus = congenital CMV infection

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76
Q

what are the problems with congenital CMV infection?

A 
thrombocytopenia purpura
DIC
microencephaly
IUGR
hepatosplenomegaly 
jaundice
chorioetinitis - inflammation of choroid of eye
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77
Q

sometimes babies with CMV infections don’t develop symptoms till 2 years. how do these children present?

A

sensorineural hearing loss
visual impairment
psychomotor developmental delay

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78
Q

what investigations can be done to confirm CMV infection?

A

serology for CMV - igG and IgM

if mother is positive for infection can test fetus via amniocentesis and PCR after 21 weeks gestation

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79
Q

what happens if a women is confirmed to have CMV infection in pregnancy?

A

cant treat mother during pregnancy because drugs are teratogenic
if fetus confirmed to have infection can offer termination or just regular monitor and support any problems.

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80
Q

what type of virus is parvovirus?

A

single DNA stranded

found in respiratory droplets or blood

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81
Q

how does parvovirus present in adults?

A

mild and self limiting or asymptomatic

sometimes get arthralgia in PIPJ or knees

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82
Q

what does parvovirus B12 infection to fetus do (pathophysiology)?

A

spontaneous miscarriage
intrauterine death

infection of erythroid system and thus replicates in erythroid progenitor cells of liver and bone marrow. this can cause:

  • severe anaemia and as a result high output heart failure
  • increased erythropoiesis by liver and extrahepatic which can result in portal HTN and hypoproteinuria.
  • hypoproteinuria in turn can result in ascites = fetal hydrops

main risk is fetal hydrops = abnormal accumulation of fluid in 2 or more fetal compartments
- ascites, subcutaneous oedema, pleural effusion, pericardial effusion, scalp oedema and polyhydramnios (all can be detected on USS)

83
Q

how does parvovirus affect children?

A

malaise, URTI, low grade fever, headache

slapped cheek

84
Q

how is parvovirus in pregnancy investigated?

A 
serum IgM (recent infection)
serum IgG (past infection and immunity
85
Q

how is parvovirus in pregnancy managed?

A

maternal infection - no treatment required
fetal infection:
- refer to fetal medicine specialist
- serial USS starting at 4 weeks post infection and repeat every 1-2 weks until 30 weeks gestation

86
Q

what type of virus is rubella?

A

single stranded RNA

airborne droplets

87
Q

what are the clinical features of maternal rubella infection?

A

often asymptomatic

may have malaise, headache, coryza, lymphadenopathy and maculopapular rash

88
Q

what does transmission of rubella infection from mother to fetus depend on?

A

depends on gestational age

highest risk early on (<12 weeks) and then gradually reduces

89
Q

what does congenital rubella syndrome consist of?

A

present at birth:

  • sensorineural hearing loss
  • cardiac defects - pulmonary stenosis, PDA, VSD
  • ophthalmic defects - retinopathy, congenital cataracts
  • CNS abnormalities - microcephaly and learning disability
  • haematological - thrombocytopenia, blueberry muffin appearance

late onset:

  • diabetes
  • thyroiditis
  • Growth hormone abnormalities
  • behavioural problems
90
Q

what investigations should we do if we suspect rubella infection?

A

ELISA for following Ab:

  • IgM Ab for rubella - present in acute infection
  • IgG ab - present following infection or vaccination

amniocentesis and PCR to detect fetal infection

91
Q

Is routine screening for rubella infection recommended?

A

no because of MMR vaccine there is now low prevalence

92
Q

how is rubella infection in pregnancy managed?

A

no treatment for mum unless fever then give anti-pyretic

fetus: if infection offer termination or USS surveillance to detect complications

93
Q

what type of virus is varicella zoster infection?

A

DNA virus

94
Q

is varicella zoster infection in pregnancy common/uncommon and what is the outcome?

A

uncommon because most people have had chicken pox

if it does occur increased mortality/morbidity for mum and fetus

95
Q

what are the clinical features of varicella zoster infection in pregnancy?

A

fever, malaise, pruritic maculopapular rash which can become vesicular and crusts then heals
can lead to hepatitis , pneumonia and encephalitis

96
Q

what should you do if mother has been in contact with chicken pox but not previously infected?

A

check IgG to test for immunity
if not immune give varicella zoster immunoglobulin (VZIG) within 10 days of contact and before rash appears (no benefit if rash already appeared)

97
Q

how should varicella zoster infection in pregnancy be treated (rash already appeared)?

A

aciclovir within 24 hours of rash onset and at >20 weeks gestation
refer to fetal medicine specialist and give serial USS beginning at 5 weeks post infection

98
Q

what should we do for women who are seronegative for varicella zoster Ab pre-pregnancy or post partum?

A

vaccine

99
Q

how is varicella zoster infection of newborn treated?

A

VZIG +/- aciclovir

100
Q

what are complications of varicella zoster infection of new born?

A

may be asymptomatic

develop chickenpox

101
Q

what increases risk of new born chicken pox infection?

A

if maternal chickenpox is in last 4 weeks of pregnancy there is significant risk of new born infection

transmission via transplacental, transvaginal or direct contact after birth

102
Q

what is fetal varicella syndrome?

A

RARE condition - caused by reactivation of varicella in utero (relies on fetus having already been infection in first 20 weeks of pregnancy)

however can lead to varicella zoster syndrome

- skin scarring in dermatomal distribution 
- eyes - cataracts, opic atrophy, micropthalmia, chorioenitis
- hypoplasia of limbs 
- neurological abnormalities = microcephaly, cortical and spinal atrophy, seizures and horners syndrome
103
Q

what treatment is recommended for those who have autoimmune conditions and are pregnant?

A 
aspirin 75mg 
(because autoimmunity increases risk of pre-eclampsia)
104
Q

how should IBD be managed during pregnancy?

A

need to sure diet is good and nutrition because it will affect the babies growth.
need to do more scans - for growth
check B12, folate, FBC, iron levels

105
Q

Those who have sickle cell and are pregnant are at risk of what?

A 
anaemia
HTN
infection
VTE
crisis 
miscarriage
IUGR
still birth
prematurity
106
Q

how is HIV transmitted to the fetus?

A

transplacental
during delivery
breast feeding

107
Q

what are the risk factors that increase maternal transmission of HIV to fetus?

A 
smoking 
viral load 
CD4 count
infection during pregnancy
Chorioamnionitis 
HIV core antigens 
other STDs 
vaginal delivery 
instrumental delivery
preterm
amniocentesis
108
Q

what factors reduce risk of fetal transmission of HIV?

A

C section
zidovudine
higher levels of HIV antibodies

109
Q

How is HIV in pregnancy managed?

A 
antiretroviral therapy (ART) - combination of 3 drugs
    - zidovudine is indicated and if viral load is very small it can be used as monotherapy

C section
no breast feeding
zidovudine given to baby 6 weeks after delivery
may require pneumocystic pneumonia prophylaxis

110
Q

what are the indications of a C section in HIV infected mothers?

A

zidovudine alone
ART + viral load >400
Hep C infection too

111
Q

what are the pros and cons of antiretroviral therapy in pregnancy?

A

pros - helps to reduce transmission of HIV to fetus

risk of drug toxicity to fetus
can cause anaemia, and liver problems and increases risk of diabetes
thus people on ART need OGTT at 24-28 weeks and iron supplements

112
Q

what are the complications of HIV infection in pregnancy?

A 
Preterm
IUGR
still birth 
low birth weight 
chorioamnionitis 
reduced fertility 
drug toxicity
113
Q

what happens to women with pre-existing asthma in pregnancy?

A

some get worse
some get better
some stay the same

114
Q

what are the complications of having asthma in pregnancy?

A

mucosal oedema and secretions mean that asthmatics are more prone to respiratory infections and pneumonia during pregnancy

pre-eclampsia / HTN
hyperemesis gravidum
uterine haemorrhage 
preterm labour and prematurity, low birth weight, IUGR
congenital abnormality - cleft lip

also neonatal hypoxia and seizures

115
Q

what are the risk factors for asthma exacerbations during pregnancy?

A

stopping medication
viral infection
smoking
stress

116
Q

what are the differentials for an acute exacerbation of asthma during pregnancy?

A

P.E
amniotic fluid embolism
aspiration pneumonitis

117
Q

how do we treat asthma in pregnancy?

A

stepwise management:

  1. inhaled salbutamol
  2. low dose inhaled steroid
  3. LABA or high steroid dose
  4. LABA and high steroid dose.
  5. oral steroids

monitor spirometry monthly and PEFR twice daily

118
Q

what effect do the following medications have on fetus?

  • theophylline
  • B2 agonists
  • corticosteroids
A

theophylline - fetal tachycardia and vomiting

B2 agonist - tachycardia, hypoglycaemia

corticosteroids - cleft palate, low birth weight, preterm, pre-eclampsia

119
Q

why are asthma attacks during labour rare?

A

hormones released

120
Q

how does pregnancy affect epilepsy?

A

sometimes can be better, sometimes worse, sometimes no change

main reason for worsened control is tiredness, fatigue and pain during pregnancy
but also pregnancy affects efficacy of AED, may have changed AED for pregnancy etc
increased risk of sudden unexpected death in epilepsy

121
Q

how does epilepsy affect pregnancy?

A

absence or partial seizures have little effect on fetus
however tonic clonic are more risky and can lead to hypoxia especially in T3 when fetal O2 requirements are higher.

increased risk of:

  • preterm, miscarriage, IUGR , fetal injury
  • APH, early separation of placenta and uterus,
  • HTN
  • deceleration on CTG
122
Q

how do we treat a seizure during labour?

A

benzodiazepines to reduce risk of fetal hypoxia and acidosis

123
Q

which AED has higher risk of NTDs than others?

A

sodium valproate= highest risk = should not be used

lamotrigine and carbamazepine are safest

124
Q

How is epilepsy during pregnancy managed?

A

Warn epileptic patients to use contraception and inform GP when wanting to get pregnant

  • medication can be altered if needed (use lamotrigine/ carbeamazepine, not sodium valproate)
  • start taking 500mg of folic acid before pregnancy and continue throughout

serial fetal growth scans indicated
IM vitamin K - reduces risk of haemorrhagic disease of new born

125
Q

which drug should be avoided in young girls with epilepsy?

A

sodium valproate

126
Q

can a mum breast feed on AEDs?

A

yes, some risk of developmental issues but benefit of breast feeding outweighs these.

127
Q

how does pregnancy affect pre-existing diabetes?

A

increased risk of complications e.g. ketoacidosis, hypoglycaemia, retinopathy, progression to nephropathy

128
Q

what are the obstetric complications of diabetes?

A 
HTN, pre-eclampsia 
thromboembolism 
still birth, premature, abortion 
shoulder dystocia, polyhydramnios 
maternal infection - UTI
129
Q

how are women with pre-existing diabetes managed in pregnancy?

A

ensure they have good glycaemic control before getting pregnant. good nutrition before and during and after
stop oral hypoglycaemics - can use metformin, glibenclamide and insulin
ACEi and statins should be stopped

130
Q

what are the glucose targets of diabetic patients in pregnancy

A

fasting = 5.3mM
after meal = 7.8mM
2 hours later = 6.4mM

131
Q

What is a contraindication to antenatal steroids?

A

Diabetes

132
Q

can oral hypoglycaemics be used during breast feeding

A

no

use metformin or glibencamide

133
Q

what is obstetric cholestasis?

A

defined as abnormal LFTs and pruritic in absence of a rash during pregnancy which is resolved by delivery

134
Q

what are the risk factors for obstetric cholestasis?

A 
previous obstetric cholestasis
FHx obstetric cholestasis 
multiple pregnancies
Hep C 
presence of gall stones
135
Q

what are the complications of obstetric cholestasis?

A

fetal distress which can result in meconium passage, preterm or interuterine fetal death
maternal comorbidity from lack of sleep

136
Q

how does obstetric cholestasis present?

A

pruritis - especially of hands and soles of feet, usually worse at night (but note that itching can occur in normal pregnancy)
may be malaise and tired
typically presents in T3
may have pale stools, dark urine and jaundice

137
Q

how do we investigate for obstetric cholestasis?

A

LFTs - raised AST and ALT and gGT
USS to rule out gall stones or fatty liver of pregnancy
can test for CMV/EBV

could it be due to any medication?

138
Q

what are differentials for obstetric cholestasis?

A

HELLP syndrome
fatty liver of pregnancy
autoimmune hepatitis

139
Q

how is obstetric cholestasis managed?

A

regularly check LFTs weekly and then 10 days post delivery
ursodeoxycholic acid

problems increase from 37 weeks plus so could consider induction of labour

140
Q

what CVS drugs are contraindicated in pregnancy?

A

ACEi, ARB, amiodarone, nitroprusside

141
Q

why is smoking contraindicated in pregnancy?

A

CO binds fetal and maternal Hb more strongly than O2 and thus reduces oxygen carrying capacity
nicotine causes vasoconstriction of uteroplacental circulation and thus reduces blood flow
smoking alters placental structure and trophoblasts - calcification
smoking has shown to reduce birth weight and crown rump length

at increased risk of PROM, preterm, perinatal mortality, placental abruption, placenta praevia, low birth weight, miscarriage

142
Q

how does smoking alter risk for pre-eclampsia?

A

reduces risk of pre-eclampsia but if happen to get pre-eclampsia then increased risk of perinatal loss.

143
Q

how are smokers helped during pregnancy?

A

offered advise and smoking cessation programme

144
Q

why is alcohol contraindicated in pregnancy?

A

fetus is at risk of fetal alcohol syndrome

145
Q

what are obese women at risk of in pregnancy?

A

miscarriage, preterm, IUGR, macrosomia, still birth

Pre-eclampsia, thromboembolism, gestational diabetes, cardiac disease, HTN

need for C section, need for forceps

PPH, shoulder dystocia

146
Q

what defines a prolonged pregnancy?

A

> 42 weeks gestation

147
Q

what are the risk factors for prolonged pregnancy?

A 
previous prolonged pregnancy 
FHx of prolonged pregnancy
nulliparous 
obesity 
maternal age >40
148
Q

what are the complications of prolonged pregnancy?

A

fetal acidaemia and meconium passage
growth restriction due to placental deficiency
- neonatal hypoglycaemia due to depletion of glycogen stores.
- increased risk of still birth
or macrosomia - need for instruments or C section

149
Q

what are the clinical features of a prolonged pregnancy?

A 
macrosomia  or static growth
oligiohydramnios 
reduced fetal movements
passage of meconium 
dry flakey skin with reduced vernix
150
Q

how do we manage a prolonged pregnancy?

A

NICE recommended offering to help with delivery by 42 weeks to prevent still birth:

  • membrane sweep offered
  • induction of labour offered 41-42 weeks

if mum refuses then biweekly CTGs required to assess for fetal distress
in event of fetal distress it may be necessary to conduct emergency C section

151
Q

what is the anatomical difference between having monozygous or dizygous twins in utero?

A

dizygous twins each have their own placenta- 2 amnions, 2 chorions

monozygous may:

  • 2 chorions, 2 amnion
  • 1 placenta , 1 chorion and two amnions
  • 1 placenta, 1 chorion , 1 amnion
  • conjoined twin

for monozygous all depends on when the zygote divides. the earlier it divides the more components which are doubled.

152
Q

what arrangements are put in place for delivery of twins?

A

monochorionic = elective C section at 36 weeks offered. steroid course given

dichorionic = elective C section from 37 weeks

triplets = elective C section from 35 weeks and steroid dose given

153
Q

when is a tertiary level care of fetal medicine required in multiple pregnancies?

A

when monochorionic monoamniotic twins

any triplets

154
Q

what is twin twin transfusion syndrome?

A

when twins share chorion there is risk of one twin getting a stronger blood supply and thus more nutrients than the other. this can affect growth of the other and in some cases the other twin dies and is absorbed in first half of pregnancy

155
Q

what are the risk factors to having a twin pregnancy?

A

family history (on maternal)
older women
previous twins
assisted conception

156
Q

what symptoms make indicate a twin pregnancy?

A

hyperemesis

large abdomen

157
Q

why is it important to check the position of twins?

A

important to keep checking because once the first twin is delivered the lie of the second can change and

C section advised in monoamniotic or non-cephalic lie of first tiwn

158
Q

what are the possible complications of twin pregnancies?

A

problems for baby: risk of preterm, miscarriage, still birth, IUGR and congenital defects

problems for mum: pre-eclampsia, anaemia, obstetric haemorrhage,

increased symptoms of pregnancy: hyperemesis gravidum, breathlessness and gord

159
Q

what are the causes of bleeding in early pregnancy <20 weeks?

A

AGE IS LO:

  • abortion, miscarriage
  • Gestational trophoblastic neoplasia
  • ectopic pregnancy
  • Implantation bleeding
  • spotting
  • lower vaginal problems
  • other e.g. cervical or urethral bleeding
160
Q

what are the causes of bleeding in later pregnancy?

A

antepartum haemorrhage
= bleeding after 24 weeks gestation
mainly caused by placenta praevia and placental abruption. can also be caused by placental rupture

bleeding from fetus is rare but can occur in vasa previa

161
Q

What approach should be taken in obstetric collapse?

A

A to E and call for help

  • 2 large bore cannulas and take bloods - FBC, UEs, LFTs, clotting, G+S
  • fluids - use hartmans (NaCl has risk of pre-eclampsia)
  • rule out Hs and Ts especially haemorrhage and P.E
  • treat any specific causes e.g. MgSO4 toxicity - give calcium gluconate
162
Q

what are the Hs and Ts that you should work through for obstetric collapse?

A

Hypovolaemia - haemorrhage (APH, ectopic pregnancy), hypotension (supine hypotension, sepsis)
Hypo/Hyper K = pre-eclampsia can cause hypoK
hypoxia / acidaemia = sepsis
hypothermia

Tension pneumothorax
Tamponade
thromboembolus - P.E, amniotic fluid embolis
Toxins

others eclampsia/seizures

163
Q

explain the pathophysiology behind red blood cell isoimmunisation

A

during pregnancy fetal blood cells can enter maternal circulation during delivery, APH, or abdominal trauma. These RBC may have different antigen compared to mother (particularly important antigen are rhesus D and ABO). The mothers immune system will be activated and produce Abs against these antigen. This is the sensitising event and usually isn’t a problem in this pregnancy.

however now the mother has Abs against that antigen, if that antigen is present in subsequent pregnancies, maternal Abs can cross placenta and attack fetal RBC causing haemolysis and anaemia

therefore rhesus isoimmunisation is possible if mother is rhesus negative and baby is rhesus positive. IF second child also is rhesus positive - attack.

164
Q

what investigations can be done to prevent red blood cell isoimmunisation?

A

check maternal Ab, antigen and blood group.
if rhesus negative = prophylaxis used to prevent sensitisation and protect future pregnancies

feto-maternal haemorrhage test = after a sensitising event (APH), the fetal RBC in maternal circulation can be measured such that the amount of antiD prophylaxis can be altered accordingly

165
Q

what is the treatment for rhesus negative mothers to prevent red cell isoimmunisation?

A

anti D Ig - binds rhesus D antigen on fetal RBC in maternal circulation to prevent maternal immune response against them

166
Q

when is anti D prophylaxis given?

A

at 28 and 34 weeks

additional dose if any of the following sensitising events take place:

  • miscarriage, ectopic pregnancy, termination of pregnany , intrauterine death.
  • amniocentesis/ chorionic villus sample, C section, delivery , external cephalic eversion
  • APH, fall/abdo trauma
167
Q

what are the contraindications to anti-D prophylaxis?

A

allergy

168
Q

how much anti-D prophylaxis should be given following a sensitising event?

A

<20 weeks a minimum of 250 U
>20 weeks a minimum of 500 U

give 125 U more for every 1ml above 4ml on the fetomaternal haemorrhage test (FMH)

always should be given within 72 hours of the sensitising event.

169
Q

What should be done after delivery in rhesus negative mum?

A

check fetal blood and if rhesus positive give mum atleast 500IU (check FMH test) of anti D Ig within 72 hours

170
Q

what are the indications to anti-D prophylaxis in <12 weeks pregnancy?

A

ectopic, termination, molar pregnancy , heavy uterine bleeding

171
Q

what stage in pregnancy feto maternal haemorrhage (FMH) testing required?

A

only after 20 weeks (before 20 weeks just give standard 250 IU of anti D Ig)

172
Q

what are the complications of iso red cell immunisation to the fetus?

A

haemolysis leading to

- anaemia 
- jaundice and possibly kernicterus
- fetal hydrops 
- possibly fetal death in utero
173
Q

what advice is given regarding anti D Ig prophylaxis and vaccines?

A

given 3 weeks before or 3 months after a vaccine

this is because it can interfere with the effectiveness of some vaccines.

174
Q

what is placental abruption?

A

this is where the placenta detaches from the uterus prematurely.
it is a major cause of antepartum haemorrhage (and also a cause of PPH)

175
Q

what is the pathophysiology behind placental abruption?

A

It is thought to occur when maternal vessels in basal layer rupture resulting in accumulation of blood between placenta and basal layer of endometrium.
the detachment of the placenta results in inability to function and thus rapid fetal compromise.
more over the blood loss can result in maternal haemodynamic instability

176
Q

what are the risk factors of placental abruption?

A 
previous placental abruption
pre-eclampsia 
abdominal trauma 
thrombophilias 
abnormal tie e.g. transverse
polyhydramnios 
smoking/cocaine 
multiple pregnancies
177
Q

what are the clinical features of placental abruption?

A 
painful vaginal bleeding 
tense, tender lower abdomen and woody uterus. 
reduced fetal movements
maternal hypovolaemic shock
fetal distress - hypoxia/death
178
Q

what are the differentials for placental abruption?

A

placenta praevia
vasa praevia
marginal placental bleed
uterine rupture

179
Q

how should placental abruption be investigated?

A

bloods: FBC, clotting, G+S/Xmatch 4 U, (LFTs and UEs - exclude HELLP syndrome and pre-eclampsia)

Kleihauer test

USS - may see retroperitoneal haematoma (good positive predictive value i.e. can confirm presence, but poor negative predictive value i.e. not good at excluding)

assess fetal well being - if >26 weeks perform CTG

180
Q

what is the Kleihauer test?

A

feto-maternal haemorrhage test = looks at amount of fetal blood in maternal circulation. this is usually to estimate the amount of anti-D prophylaxis required in rhesus negative women.

181
Q

what examination is contraindicated if placental praevia is suspected?

A

vaginal examination - can increase bleed.

182
Q

how is placenta praevia managed?

A

A to E

  • high flow O2
  • cannula and fluids to get systolic >100
  • catheterise

if maternal/ fetal compromise - delivery of fetus usually by C section (quickest method)
if no maternal/ fetal compromise but at term then induce labour
conservative if no maternal/fetal compromise and not at term = usually for partial or marginal abruption

all rhesus negative women are given anti D prophylaxis within 72 hours of bleeding onset.

183
Q

what is placenta praevia?

A

partial or full attachment of placenta to lower uterine segment

184
Q

what are the two types of placenta praevia?

A

minor placenta praevia - attached to lower uterine segment but doesn’t cover the internal cervical os

major placenta praevia - covers internal cervical os

185
Q

what are the two types of placenta praevia?

A

minor placenta praevia - attached to lower uterine segment but doesn’t cover the internal cervical os

major placenta praevia - covers internal cervical os

can also be divided into 4 types:
type 1 - in lower 1/3 near cervical os
type 2 - reaches edge of cervical os
type 3 - placenta partially covers os
type 4 - completely covers os

186
Q

what is the problem with placenta praevia?

A

low lying placenta is more at risk of haemorrhage due to defective attachment to uterine wall. this bleeding can be spontaneous or provoked (minor trauma). Therefore major cause of APH and also PPH

not usually a problem for fetus but risk to mother

associated with

  • placenta accreta
  • placenta increta
  • placenta percreta
  • vasa praevia
187
Q

what is placenta accreta?

A

blood vessels and other parts of placenta grow more deeply into the uterine wall. Detachment from uterine wall after delivery is more difficult and can result in PPH

188
Q

what is placenta increta?

A

blood vessels are deeply attached to muscular uterine wall (more so than placenta accreta) and this prevents separation at birth

189
Q

what is placenta percreta?

A

placenta attaches itself and grows through the uterus and sometimes extending into nearby organs - bladder

190
Q

what 3 abnormalities with the placenta increase risk of PPH?

A

placenta acreta
placenta increta
placenta percreta

191
Q

what is vasa praevia?

A

fetal blood vessels cross or run near the opening of the uterus.
these vessels are thus at risk of rupturing when membranes rupture.
if these rupture, fetal blood is lost (more significant because less fetal blood available)

can result in bradycardia, hypoxia and need for urgent delivery

192
Q

what are the risk factors for placenta praevia?

A 
previous C section - main risk factor
previous placenta praevia 
maternal age >40
high parity
multiple pregnancy 
endometritis 
curettage of endometrium after a miscarriage/termination
193
Q

what are the clinical features of placenta praevia?

A

painless vaginal bleeding
soft non tender uterus on palpation
may see a c section scar

194
Q

what investigations should be done if placenta praevia is suspected?

A

bloods - FBC, clotting, G+S, X match
USS - look for short distance between lower edge of placenta and cervical os
fetal well being CTG

195
Q

how is placenta praevia managed?

A

not bleeding but been diagnosed at 20 weeks…

  • for minor repeat scan at 36 weeks (likely placenta has moved superiorly)
  • for major repeat scan at 32 weeks - plan delivery
  • all women with placenta praevia major should have an elective C section at 38 weeks.

if bleeding:

  • A to E
  • emergency C section despite gestational age - protect mum
  • anti- D prophylaxis for rhesus negative within 72 hours of bleed
196
Q

how is antepartum haemorrhage defined?

A

bleeding post 24 weeks gestation up to delivery

197
Q

what are the causes of antepartum haemorrhage?

A

placenta praevia and placental abruption are the 2 major causes

198
Q

what are the causes of antepartum haemorrhage?

A

placenta praevia and placental abruption are the 2 major causes

marginal placental bleed - small placental abruption which is large enough to cause revealed bleed but not enough to cause maternal/fetal compromise

vasa praevia
uterine rupture
local genital causes: polyp, carcinoma, cervical ectropian (common), infections

199
Q

what is the classical triad for vasa praevia

A

vaginal bleed
rupture of membranes
fetal compromise - rupture of umbical cord vessels results in loss of fetal blood and quick deterioration in fetal condition

200
Q

what questions should you ask in a history of someone presenting with APH?

A

how much bleeding and when did it start?
fresh or old blood? mucus?
pain? (important to distinguish praevia from abruption)
provoked? (post coital)
could waters have broken
fetal movements?
risk factors - smoking, domestic violence, drugs

201
Q

how is APH managed?

A

ABCDE, high flow O2, IV fluids, X match, catheter.

202
Q

what are you looking for on examination of someone with APH?

A 
signs of shock - tachycardia, hypotension 
tender abdomen
tense or soft uterus 
palpable contractions?
lie of fetus
CTG - required if 26 weeks or more.
203
Q

what should be avoided in APH?

A

speculum or vaginal examination until placenta praevia excluded on USS (if placenta praevia doing either of these could cause massive haemorrhage)

204
Q

what is pubic symphysis dysfunction?

A

pain in pregnancy due to stretching of pubic symphysis

Obstetrics (8 decks)

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