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PATHOLOGY > Obstetric haematology > Flashcards

Obstetric haematology Flashcards

1
Q

how does the full blood count change in pregnancy

q

A

mild anaemia:
* red cell mass rises (120-130%)
* plasma volume rises more than red cell mass (150%) expansion complete by end of 2nd trimester

macrocytosis
* normal
* or B12/folate def

neutrophilia - cells are normally more marginalised come into the circulation.

thrombocytopenia: Fall in plt count -> increase in plt turnover -> earlier plts released -> increase in plt size.

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2
Q

iron requirement in pregnancy

A

300mg for fetus
500mg for maternal increased red cell mass
in diet - 30g
normally absorb 1-2mg from 30mg, in preg absorb 6mg

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3
Q

consequence of iron deficiency in pregnancy

A

IUGR
prematurity
postpartum haemorrhage

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4
Q

folate requirements in pregnancy

A

increase

growth and cell division
approx additional 200mcg/day required

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5
Q

summarise the iron cycle - including the changes in pregnancy

A
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6
Q

RCOG recommendations with folate supplements

A

supplement before conception and for >= 12 wks gestation
400ug/day

reduces risk of neural tube defects

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7
Q

definition of anaemia in pregnancy

A

Hb<110 1st trimester
<105 2nd and 3rd
<100 postpartum

reduction in threshold due to dilutional effect

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8
Q

things to dx iron deficiency anaemia

A
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9
Q

summarise how the platelet count changes in pregnancy

A

Due to increased clearance - mainly in 3rd trimester
Shift in normal distribution to L

Platelet clumping - so if low plt count correlate with film

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10
Q

causes of thrombocytopenia in pregnancy

A

physiological - gestational/incidental thrombocytopenia
PET
ITP
MAHA
bone marrow failure, leukaemia, hypersplenism, DIC etc

when plts <150 - most will be gestational
<100 - splite gestational and ITP
<70 - mostly ITP, more PET than gestational

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11
Q

summarise gestational thrombocytopenia

A

physiological decrease in plt count - approx 10%
>50 is sufficient for delivery
>70 for epidural (spinal haematoma)
mechanism - unknown. dilution and increased consumption
baby not effected
plt count rises day 2-5 post delivery

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12
Q

summarise preeclampsia and thrombocytopenia

A

50% get thrombocytopenia - propirtionate to severity
due to increased activation and consumption
associated with coag activation (incipient DIC - normal PT and APTT, high factor 8) 1st thing that happens in insipient DIC )

mx is delivery

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13
Q

summarise immune thrombocytopenia in pregnancy

A

accounts for 5% of thrombocytopenia in pregnancy
can precede pregnancy
Rx - IVIG, steroids, azathioprine

baby can be effected - ab cross placenta
* unpredictable which babies effected
* check cord blood and then daily
* may fall for 5 days post preg
* bleeding in 25% of severely affected - need to give IVIG and cranial USS when baby plt count low
* consider MOD - avoid forceps/ventouse

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14
Q

summarise microangiopathic syndromes in pregnancy

A

deposition of plts in small blood vessels
thrombocytopenia
plt rich clots sheer the blood cells
fragmentation and destruction of RBC within vasculature
organ damage - kidney, cns, placenta

not effected/cured by delivery

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15
Q

eg of reasons population getting more prone to VTE

A

older
IVF
multiple preg
obesity

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16
Q

summarise the coagulation changes in pregnancy

A

Factor 8 and vWF increase until term

Protein S (anticoag) falls

PAI-2 is produced by placenta and is fibrinolytic inhibitor

Hypercoaguable hypofibrinolytic state
17
Q

why does pregnancy need to be hypercoaguable

A

Because 700ml/min is blood flow throigh placenta - need to prevent bleeding at birth

however: uterine contraction, not coag, is one of the main factors that stop bleeding at birth

18
Q

overall effects of changes in coagulation factors etc in preg

A

increased thrombin generation
increased fibrin cleavage
reduced fibrinolysis

19
Q

when is the biggest risk of VTE in pregnancy

A

Risk goes up through pregnancy - venous stasis due to gravid uterus
Hormonal changes in vessel wall
All 3 of virchows triad

Highest risk is the 6wks post delivery

20
Q

RF for VTE in preg in women who died of PE

A

BMI >25
personal/Fhx VTE
air travel
hyperemesis gravidarum -> dehydration
ovarian hyperstimulation syndrome -> upper limb fibrosis
unrelated surgery

21
Q

how do you assess VTE in pregnancy

A

Doppler and V/Q scan

22
Q

RF for thrombosis in pregnancy

A
23
Q

prevention of VTE in pregnancy

A

RFs should get prophylactic LMWH and TED - either: throughout preg, in peri-post-partum period
mobilise early
maintain hydration

24
Q

Mx of thromboembolic disease in pregnancy

A

LMWH (enoxaparin) as for non-preg, once or twice daily
doesnt cross placenta
After 1st trimester - measure anti Xa levels because LMWH more unpredictable than when pregnant
*(NOT warfarin - crosses placenta and teratogenic between wk 6-12
NOT DOAC - cross placenta and secrete in breast milk) *

25
Q

birth plan when on LMWH

A

stop for labour or planned delivery - esp epidural

epidural wait 24 hr after rx dose and 12hr after prophylactic dose

26
Q

effect of warfarin on fetus

A

Chondroplasia punctata:

abnormal cartilage and bone formation
early fusion of epiphyses
nasal hypoplasia
short stature
asplenia
deafness
seizures

27
Q

summarise antiphospholipid sundrome

A

recurrent miscarriage and persistent lupus anticoagulant (LA) (ie 12wks apart) and/or antiphospholipid antibodies

3 or more consecutive miscarriages before 10wks gestation

one or more morphologically normal fetal loss >10wks

one or more preterm <34wks due to placental disease

28
Q

rx of antiphospholipid syndrome in pregnancy

A

aspirin and heparin

29
Q

definition of postpartum haemorrhage

A

> 500ml blood loss

30
Q

4Ts of post partum haemorrhage

A

tone
trauma
tissue
thrombin

31
Q

mechanisms of postpartum haemorrhage

A

major:
* uterine atony
* trauma

haematological factors are minor except
* dilutional coagulopathy after resus (given red cells, not plasma)
* DIC in abruption, amniotic fluid embolism etc

32
Q

summarise pregnancy and DIC

A

coagulation changes in pregnancy to predispose to DIC
decompensation is precipitated by:
* amniotic fluid embolism
* placental abruption
* retained dead fetus
* PET
* sepsis

ie Exposure of tissue factor to activated factor 7 - these are sources of tissue factor in pregnancy

33
Q

summarise amniotic fluid embolism

A

sudden onet shivers, vomiting, shock, DIC
high mortality
presumed mech - tissue factor in amniotic fluid entering maternal blood stream
almost all >25ys
usually 3rd trimester

34
Q

what is the aim of haemoglobinopathy screening

A

Need to know whether parents are Ao carriers - need to know where in the world this is prevalent

Have 4 alpha genes - so in Ao - all 4 affected - Hb Barts - hydrops fetalis, not compatable with life
35
Q

summarise haemoglobinopathy screening in pregnancy

A

universal screening when background high prevalence
in some places - use family origin questionnaire to determine
use HLPC - to detect b thal. cant detect a thal like this (needs DNA analysis)
HLPC also identifies Hb variants
only importnat to detect alpha 0 trait

aim to complete screen by 12/40 including of partner

36
Q

summarise counselling on haemaglobinopathy

A

important disorders all recessive
so if mum heterozygous - partner should be tested
combinations as important as homozygous states
options:
* proceed
* prenatal diagnosis (CVS sampling @10-12wks, amniocentesis @15-17wks, fetal blood sampling, cell free fetal DNA)
* USS screening for hydrops

37
Q

differentiate thalassaemia trait from iron deficiency anaemia from blood tets

A
Low MCH in iron - will also have a low Hb. Can have normal Hb in thalassaemia trait

PATHOLOGY (94 decks)

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