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Pathology > Haematology of Pregnancy > Flashcards

Haematology of Pregnancy Flashcards

1
Q

is anaemia worrisome in pregnancy?

A

no

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2
Q

what happens to the blood in pregnancy?

A

due to the expanding uterus, the blood volume increases without any increase in the population of red cells, meaning that the maternal Hb is diluted

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3
Q

normal Hb parameters in pregnancy

A

booking: >12g/dl

3rd trimester: >10g/dl

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4
Q

commonest causes of pathological anaemia in pregnancy

A
  • fe-deficiency

- folate deficiency

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5
Q

how are Fe and folate deficiency anaemias managed?

A

supplements of the respective element

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6
Q

causes of increased Fe demands

A
  • increased red cell mass
  • foetus and placenta
  • blood loss at delivery
  • lactation
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7
Q

causes of increased folate demands

A
  • foetal development

- lactation

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8
Q

why doesn’t B12 deficiency occur in pregnancy?

A
  • women with pernicious anaemia find it harder to conceive

- B12 stores last years and thus, are less easily depleted

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9
Q

why is there a prothrombotic state in pregnancy?

A
  • decreased concentration of anticoagulant factors like protein S
  • increased concentration of prothrombotic factors like fibringen, factors 7, 8 and vWF
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10
Q

risk factors for thrombosis in pregnancy

A
  • increased maternal age
  • parity
  • obesity
  • bed confinement
  • oestrogens
  • operative deliveries
  • gravid uterus
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11
Q

investigations for thrombosis

A
  • doppler ultrasound
  • venogram
  • pulmonary angiography
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12
Q

investigations for PE

A
  • V/Q scan

- CTPA

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13
Q

can you use warfarin in pregnancy?

A
  • completely contraindicated in the 1st trimester as this is teratogenic
  • you can still use warfarin in 2nd/3rd trimester but use with caution
  • use of warfarin can risk the foetus suffering haemorrhage
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14
Q

which type of heparin is preferred in pregnancy and why?

A
  • low molecular weight heparin
  • convenient
  • use of lower doses
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15
Q

what condition arises if heparin is used long-term in pregnancy?

A

osteoporosis (this is reversible unless there is a very short gap between pregnancies)

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16
Q

how do you manage a patient with heparin?

A
  • start with an UFH loading dose and then use IV infusion
  • switch to SC and the dose is adjusted according to the APTT ratio
  • stop when contractions start but keep heparin handy during the delivery
  • postpartum: SC and then switch to warfarin on day 2 and keep them on it for 3m
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17
Q

when can you give an epidural?

A
  • platelets >80K
  • normal clotting
  • no heparin given in the previous 6 hours
  • if not, the mother can get an epidural haematoma
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18
Q

how are the high-risk patients?

A

those who are already on warfarin

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19
Q

why can a patient can on warfarin?

A
  • thrombophilia
  • lupus
  • mechanical heart valve
  • recurrent DVT
  • antithrombin deficiency
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20
Q

how do you manage intermediate risk patients?

A

heparin prophylaxis in the 3rd trimester and/or postpartum

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21
Q

how can you monitor LMWH?

A

anti-Xa assay

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22
Q

advantages of LMWH

A
  • does not affect APTT
  • good and predictable bioavailability
  • longer half-life
  • no monitoring
  • fixed, weight adjusted doses used
  • lower dose required
  • lower risk of ostroporosis or HIT
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23
Q

how can you do a anti-Xa assay?

A
  • collect blood 4-6hrs after you have given the dose of heparin
  • target levels differ depending on whether you want a therapeutic or a prophylactic effect from heparin
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24
Q

target levels of anti-Xa assays for heparin use

A

prophylaxis: 0.1-0.3iu/l
therapeutic: 0.3-0.6iu/l

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25
Q

what is gestational thrombocytopenia

A

physiological condition which happens due to the plasma volume expansion in pregnancy

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26
Q

characteristics of gestational thrombocytopenia

A
  • prominent in the 3rd trimester
  • mild
  • no complications for neither party
  • resolves spontaneously after delivery
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27
Q

management of gestational thrombocytopenia

A

monitor

28
Q

other causes of thrombocytopenia in pregnancy

A
  • pre-eclampsia associated thrombocytopenia
  • ITP
  • MIAHA
  • HIV-related thrombocytopenia
29
Q

which is the most common cause of thrombocytopenia per trimester of pregnancy?

A

1st: ITP
2nd: ITP
3rd: gestational thrombocytopenia

30
Q

treatment of ITP

A
  • steroids

- IV immunoglobulins

31
Q

problems with steroids

A
  • increased risk of developing DM, HTN, eclampsia and can cause psychosis
32
Q

problems with IVIG

A

with repeated usage, you can be refractory to the medication

33
Q

what foetal problem can manifest in ITP?

A

risk of intracerebral haemorrhage; avoid manipulative delivery; opt for caesarean/vaginal delivery

34
Q

what is PET?

A

pre-eclampsia toxaemia

35
Q

characteristics of HELLP

A
  • deranged LFTs

- haemolysis

36
Q

management of PET

A

cover delivery with a platelet transfusion

37
Q

what is DIC?

A

disseminated intravascular coagulation

38
Q

causes of DIC

A
  • septic abortion
  • abruptio placentae
  • eclampsia
  • amniotic fluid embolism
  • placenta previa
  • retained dead foetus
39
Q

pathogenesis of DIC

A
  • placental material is thrombogenic, which can then leak into the maternal circulation
  • this can activate white cells into clotting
  • these thrombi can settle in the capillaries of end organs, causing multisystem failure
  • there is also a bleeding tendency because of the extreme consumption of the coagulation factors and the platelets
40
Q

what happens in acute DIC?

A
  • massive activation of coagulation that overwhelms compensatory mechanisms
  • bleeding
  • end-organ failure
41
Q

what happens in chronic DIC?

A
  • continual low level or intermittent activation is compensated leading to a state where coagulation tests coagulation tests are only mildly deranged
  • bleeding tendency in procedures
42
Q

laboratory findings in DIC

A
  • platelet count (decreased)
  • INR (increased)
  • APTT (increased)
  • fibrinogen (decreased)
  • FDPs (increased)
43
Q

why can INR be elevated?

A

depletion due to the extreme consumption of factor VII

44
Q

management of DIC

A
  • FFP
  • cryoprecipitate
  • platelets
  • blood
  • APC
  • antithrombin concentrates
  • supply blood products during delivery
45
Q

how can you do antenatal diagnosis?

A
  • screening of mother and father at term
  • foetal screening done
  • foetal blood analysis
  • DNA analysis
46
Q

when can prenatal blood sampling be done?

A

late 2nd trimester onwards

47
Q

how can foetal DNA be obtained?

A
  • transplacental approach

- transabdominal approach

48
Q

which procedures actually get the foetal DNA?

A
  • amniotic fluid cells

- chorionic villous sampling

49
Q

complications of foetal DNA sampling?

A
  • spontaneous abortion
  • placental damage and haemorrhage
  • rhesus sensitisation
  • premature delivery
50
Q

why do haemolysis happen in the newborn?

A

a rhesus negative woman gives birth to a rhesus positive baby. When blood cells from the baby go into the mother’s bloodstream, the mum is stimulated to produce anti-rhesus. Since these antibodies are IgG, they can cross over into the placenta and baby’s bloodstream. These sensitise the fetal blood sense and break down the blood cells extravascular by the RES.

51
Q

which pregnancies are usually affected by haemolytic disease of the newborn?

A

the 2nd pregnancy onwards

52
Q

why are such disease rarer nowadays?

A
  • production of anti-D prophylaxis
53
Q

what is the most common cause of haemolysis in the newborn?

A

ABO incompatibility (when a O mother has a A/B/AB baby)

54
Q

which pregnancies can be affected by ABO incompatibility?

A

1st onwards (the IgG would be preformed and thus, ready for action)

55
Q

treatment for haemolytic disease of the newborn

A

exchange transfusions

56
Q

which women are sensitised, and thus more likely to suffer from haemolysis of the newborn?

A
  • miscarriages
  • antenatal procedures
  • transfusions
57
Q

how do you monitor haemolytic disease in the newborn?

A
  • maternal blood checked at booking and at 28-32 weeks (if negative, you will not be monitored further)
  • if you are positive to the antibodies, you will be monitored monthly in the 1st/2nd trimester and forenightly till term
  • routine antenatal prophylaxis
  • ultrasound (severity of the haemolytic process and bile pigments in the amniotic fluid)
58
Q

what is noted from the blood checks in haemolytic disease of the newborn?

A
  • strength of the antibodies

- rate of the rise in antibodies

59
Q

when is prophylaxis given in haemolytic disease?

A
  • it is given after delivery to rhesus negative unsensitised women
  • in an infant who is rhesus positive and cover all antenatal procedures
60
Q

what happens if there is haemolysis in the baby?

A

bile pigments accumulate in the amniotic fluid, causing placenta to swell, hepatosplenomegaly and ascites
- worse: kernicterus, intrauterine death, hydrops fetalis

61
Q

what is damaged to cause kernicterus?

A

basal ganglia

62
Q

management of haemolytic disease

A
  • phototherapy (lowers bile pigments)

- intrauterine exchange transfusion (remove bile and antibodies)

63
Q

criteria for blood to be transfused

A
  • O neg
  • CMV neg
  • irradiated
  • compatible with the mother
64
Q

what is checked in the baby after they are born?

A
  • ABO group

- DCT (autoimmune haemolytic anaemia)

65
Q

what should be checked before you give an exchange transfusion?

A
  • bilirubin level

- Hb level

Pathology (21 decks)

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