Haematological changes in Pregnancy Flashcards

1
Q

How much does Hb decline by?

A

110 -> 100 g/l

- Techincally increases in pregnancy but bigger increase in plasma volue

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2
Q

What WBCs increase the most?

A

Neutrophils

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3
Q

What is “gestational thrombocytopenis”?

A

Fall in plateltes in pregnancy to lower limit of 80-90x10^11/L

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4
Q

What is the increase in mean cell volume (MCV)?

A

4 L (eg 84 to 88)

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5
Q

What fibrinogen factors are increased to create a hypercoagulable state?

A

Factors:

  • VIII
  • IX
  • X
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6
Q

Amounts of what substance should be checked to see if a woman has iron deficiency anaemia?

A

Ferritin (MCV may be normal)

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7
Q

What are the common side-effects of iron supplementation which is often given in pregnancy?

A
  • Constipation
  • Abdo pain
  • Nausea
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8
Q

What is a type of IV iron medication?

A

Ferinject (not as common as oral)

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9
Q

What is given to reduce neural tube defects (formed in 2-4 wks post conception)?

A

400mcg/day

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10
Q

What can immune thrombocytopenic purpura (ITP) be triggered by?

A

Infection, drug or pregnancy

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11
Q

What causes immune thrombocytopenia purpura?

A

Auto antibodies to platelets (marrow normal)

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12
Q

How is immune thrombocytopenia purpura treated?

A
  • Watch and wait
  • Steroids
  • Immunoglobulins
  • Splenectomy
  • Drugs to mimic thrombopoetin
  • Fetal scalp sample can be taken to check if IgG antibodies have crossed from placenta to cause ITP in fetus
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13
Q

What is Thrombotic Thrombocytopenc Purpura (TTP)?

A
  • Rare but life-threatening “thrombotic microangiopathy”
  • Enzyme ADAMS13 prevents large Von Willebrands polymers - this becomes deficient and platelets aggregate
  • Present as fever, neurological and renal disease, low platelets and fragmented red cells. Coagulation screen usually normal
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14
Q

What enzyme causes TTP?

A

ADAMS13

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15
Q

What is Thrombotic thrombocytopenic purpura associated with?

A

Auto-immune disease, HIV, pregnancy

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16
Q

How is thrombotic thrombocytopenic purpura treated?

A

Plamsa exchange (to replace ADAMS13)

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17
Q

What is the UK maternal death rate in pregnancy?

A

9 per 100,000

18
Q

What is the leading cause in the UK of maternal death in pregnancy

A

Pulmonary embolism `

19
Q

What is the high-risk area for thromboembolic disease?

A
  • Pregnancy plus 6 weeks post-partum (hypercoagulable state)
20
Q

What factors increase the risk of thromboembolic disease?

A
  • Age
  • Previous clot
  • Smoking
  • Twins
  • Obesity
  • Thrombophillia eg anti-thrombin deficiency
21
Q

What is thought to cause leg swelling in pregnancy?

A
  • Pelvic veins being compressed in late pregnancy (L>R)

- Can also lead to DVT

22
Q

How can thromboembolisms be diagnosed?

A
  • Doppler exam of leg
  • CXR - if abnormal CT pulmonary angiogram (higher radiation dose) more reliable than ventilation/perfusion scan
  • NOT D dimers
23
Q

How is thromboembolic disease treated in pregnancy?

A
  • Low molecular weight heparin
  • Increase rate of clearence and volume of distribution requires twice daily dose
  • Monitoring of anti Xa levels (3-4 hours post dose) required to show effective dosing
  • Will need prophyactic anticoagulation in future pregnancies
24
Q

What can PET lead to in a minority of cases?

A

HELLP

  • Haemolysis (anaemia, red cell fragments, raised LDH)
  • Elevated liver enzymes
  • low platelet count
25
What are the risk factors for a major haemorrhage ante or post- partum?
- Placenta praevia (over cervix) - Placental abruption - Retained products of conception - Poor uterine contraction after delivery
26
How are major haemorrhages treated?
Treat the cause and replace red cell/platelets/coagulation factors
27
What are the Wilson and Junger screening criteria?
- Recognisable latent or early symptomatic stage - A simple test with high sensitivity and specificity - Test should be acceptable to the population - Early effective treatment needs to be clear of benefit - Agreement as to who should be treated - Condition is an important health problem - Diagnosis an treatment should be cost-effective - Case finding should be a continous process - Natural history should be understood - It should be cost effective in relation to overall health-care expenditure
28
Why is Scotland considered "low prevalence" for haemoglobinopathies and thalassemia?
Low asian and afro-caribbean populations
29
What makes up heamoglobin (HbA)?
- 2 alpha-like chains | - 2 beta-like chains
30
What other haemoglobins are present in the adult blood other than HB A and what are they made up of?
- Hb A2 = 2 alpha, 2 delta (2.5%) | - Hb F (foetal) = 2 alpha, 2 gamma (0.5%)
31
What chromosome codes for the alpha-like chains?
16
32
What chromosome codes for the beta-like chains?
11
33
What will the MCV be like in individuals with a haemoglobinopathy or thalasemia?
Microcytic MCV < 80 and mean cell Hb < 27
34
How can haemoglobinopathy or thalasemia be diagnosed?
- Ethnic origin - Microcytic - Blood film - target cells in thal heterozygous , sickle slide test - Cellulose acetate or agarose gel Hb electrophoresis - High performance Liquid Chromatography (HPLC) - Gene copy number - Gene sequencing
35
What will abnormal haemoglobins show on?
Electrophoresis/HLPC
36
What will HbA2 be in beta thal heterozygous?
>3.5% (also low MCV and MCH)
37
What will alpha thalasemia with 1 deletion show?
- No change, 2 deletions, low MCV | - Gene copy number or sequencing may be needed
38
How is pre-natal screening done for haemoglobinopathy or thalasemias in low prevelance areas?
- FBC (approx 12 wks) - is MCH <27pg? - Family origin q's for both parteners - If either positive then HPLC ook for thal/haemoglobinopathy - May need confirmaatory tests - May need to check partner's FBC etc (beware non-paternity)
39
What is consodered igf foetus is at risk of serious Hb disorder?
- 11-14 wks chorionic villous sampling for foetal DNA or 15 wks + amniocentresis - Possible termination? - Newborn screening includs sickle cell disease on heel prick
40
What are the embryonic globins?
- Zeta which is replaced by alpha | - Episilon replaced by gamma then delta then beta