haematology in pregnancy

Question 1

During pregnancy what happens to: iron HB platelets neutrophils

Answer 1

Iron demand increases due to fetus (+increase maternal red cells). may lead to iron deficiency as preferential to fetus (IUGR prematurity postpartum haemorrhage).

Hb concentration stays the same as red cell mass (120% rises but so does plasma volume ((150%) mild aneamia

platelet count falls. increase platelet size, thrombocytopenia, gestational (third trimester) will resolve post partum. also increased risk of other thrombocytopenias neutrophils increase

Question 2

Thrombocytopenai causes during pregnancy

Answer 2

gestational /physiological (dilution + increased consumption)

pre-eclampsia (increased activation and consumption)

ITP (pregnanchy is a immune suppresive state, immune conditions can be unmasked)

MAHA (TTP HUS)

extent of failure is important <150 gestational <70 ITP/preclampsia

Question 3

ITP in pregnancy treatment

Answer 3

5% thrombocytopenia pregnancy is a immunomodulatory state

first trimester

IVIG, steroids anti-D if RhD +ve

baby can be affected can cross placenta IgG

check cord blood

may fall 5 days af

Question 4

coagulation changes in pregnancy

Answer 4

hypercoaguable state

VTE is leading cause of mortality

rise in procoagulants factor8 vWF, fibrinogen, factor7

fall in anticoagulant protein S

hypofibrinolytic

PAI-1

PAI-2

plasminogen activation inhbitor increases

PAI-2 only placental production

obesity big risk factor 1/3 are postpartum

Question 5

risk factors for thromboembolic disease in pregnancy

and prevention

Answer 5

coagulation reduced venous return (left DVT)

dehydration b

bed rest

obesity >29 3x risk PE

operative delivery

previous vte

increasing age

parity more kids

women with high risk factors should recieve prophylactic heparin + TED stockings

Question 6

VTE management during pregnancy contraindication

Answer 6

do not give warfarin as it crosses placenta tetarogenic also new oral anticoagulants can cross placenta

LMWH (stop during delivery)

Question 7

cardiolipin and lupus anti coagulant

Answer 7

anti phospholipid syndrome (APLS)

recurrant msicarrage, three or more consecutive miscarriages before 10 weeks.

Question 8

post partum haemorrhage mechanisms

Answer 8

uterine atony (syntocin drug)

trauma

DIC in abruption preclampsia

Question 9

what causes DIC in pregnancy and increased by misoprostol 3rd trimester

Answer 9

amniotic fluid embolism used to be fatal, high in procoagulants due to tissue factor

Question 10

if mother is hetrozygous for haemoglobinopathy what should you do?

Answer 10

test partner as fatal disorders are recessibe

Question 11

chromsome for alpha thalasaaemia and 4 types

Answer 11

chromsome 16 , 2 copies 2 loci ie.4 alpha genes

a thal trait 3 copies

a thal minor 2 copies asymptomatic low MCV

haemoglobinH disasese, Haemotetramers formed insoluble hepatosplenomegaly , moderate severe haemolytic anaemia, Heinz bodies .. unpaired B chains , b4 tetramers in RBC

Hb Barts hemotetramers no effective erythropoeisis , Hydrops fetalis, gamm4 tetramers cannot deliver oxygen

Question 12

Iron defieicny vs thalassaemia trait in preganancy

Answer 12

microcytic hypochromic picture in both

MCHC are low in iron defiency

RDW increased in iron (reticulocytes) normal in thalasaaemia

RBC low/normal, thalasaaemia increased

Hba2 increased in bthal trait

Question 13

b Thalassaemia chromsome and types

Answer 13

chromosome 11 splicing defect italy

can be heterozygous or homozgous major/minor

microcytic rbc asymptomatic or mild anaemia

electrophoresis HbA2 HbF

no b-globin production –> alpha globin production haemotetramers , extramedullary hyperplasia hepatosplenomegaly , chipmunk facies

blood transfusion however iron overlated need chelation

jaundice