1. a) T b) F c) T d) F e) F
Current available evidence suggests that pre-conceptual low Hb is associated with the delivery of low birth weight babies. There is no evidence to support any possible beneficial effects either to the mother or the fetus from high protein supplements during pregnancy. Daily antenatal oral iron supplements containing 60 mg of elemental iron have been shown to be safe and effective in reducing anaemia at term even in areas with high malaria transmission. Weekly iron supplements are not recommended for anaemic pregnant women. Anthelmintics are indicated only if helminthiasis is diagnosed or in areas of high helminthiasisprevalence.
2. a) T b) F c) F d) F e) F
A serum ferritin (SF) of 4 μg/L is well below the normal range (> 12 μg/L). In the presence of underlying inflammatory conditions the SF may be increased even up to 50 μg/L. A non-anaemic woman can be iron deficient. Microcytosis of Iron deficiency will not be detected if there is co-existing folate and or vitamin B 12 deficiency, and pregnancy induced macrocytosis. The mean corpuscular volume is an average quantity. Current available evidence suggests that weekly oral supplements of 60 mg of iron are inadequate to meet the additional requirement of pregnancy in iron deficient women.
3. a) F b) F c) T d) F e) F
Iron supplements are best absorbed on an empty stomach. A full stomach withphytates and polyphenolic compounds will reduce the unpleasant side-effects. However the absorption will be reduced. Iron absorption is inhibited by tea, coffee and calcium, and enhanced by vitamin C in orange juice. Immune thrombocytopenia has no effect on iron metabolism or iron stores. There is currently no definite evidence that iron supplements increase susceptibility to infection and the anaemia of chronic renal disease needs treatment with haematinics.
4. a) F b) T c) F d) F e) F
Anaemia appearing at 36 weeks in a previously non anaemic woman indicates she has iron deficiency (ID) which will lead to ID in the new born and all its associated adverse effects during infancy, childhood and adolescence. If not treated she may not be able to tolerate even a moderate post partum haemorrhage and thus carries an increased risk of mortality. Daily oral supplements containing 60 mg of elemental iron and 400 μg of folic acid and a good nutritious diet can improve the Hb adequately prior to delivery. An anthelmintic may be required. She is unlikely to deliver at 36 weeks gestation. A packed cell transfusion may be considered in low resource settings if the Hb is < 9.0 g/ dL at term. In well resourced settings where recombinant human erythropoietin is available, it may be indicated if the Hb is < 7.0 g/ dL (not <9.0 g/ dL) and she declines a packed cell transfusion.
5. a) T b) F c) F d) T e) T
Both parents have sickle trait, therefore they have a 1 in 4 chance of having a baby with HbSS – homozygous sickle cell disease, if the baby inherits the S gene from both parents. They also have a 1 in 2 chance of having a baby with sickle trait (AS) if the baby inherits the A gene from one parent and the S gene from the other parent, and 1 in 4 chance of having an unaffected child (AA) if the baby inherits the A gene from both parents. The child will inherit an S gene from the mother and an A gene from the father, so all children will have sickle trait (AS). 1 in 2 offspring from couple b will have sickle trait (AS) if they inherit the S gene from the mother and the A gene from the father. 1 in 2 offspring will be AA, if they inherit the A gene from both parents. 1 in 4 offspring will be a compound heterozygote of HbS and HbC, (HbSC) and will have SCD, inherited the S gene from the mother and the C gene from the father. 1 in 4 offspring will be HbC trait (AC) and 1 in 4 offspring will have sickle trait (AS). 1 in 4 offspring will be unaffected (AA). Similar to d, 1 in 4 offspring will have SCD, being a compound heterozygote of HbS and bthalassaemia (HbSbthalassaemia) having inherited the S gene from the mother and the b thalassaemia gene from the father. 1 in 4 offspring will have sickle trait (AS), 1 in 4 will have b thalassaemia trait and 1 in 4 will be unaffected (AA).
6. a) T b) F c) T d) F e) F
a and c are appropriate initial treatment for an acute painful sickle crisis. Fluids can be given orally, or intravenously if oral intake is poor. Analgesia should be given rapidly, commencing with simple analgesia such as paracetamol, co-codamol or dihydrocodeine, if these have not already been given at home. If these are not sufficient, strong analgesics such as morphine should be given orally or parenterally depending on patient preference. Blood transfusion is not recommended initial treatment of sickle crisis, but may be required if the painful crisis is associated with a marked anaemia, or if pain is persistent or recurrent. Steroids are not of benefit in the treatment of painful sickle cell crisis. Hydroxycarbamide is used for the prevention of acute painful sickle crisis, not for its acute management and this drug should not be used in pregnancy because of teratogenicity.
7. a) F b) T c) T d) F e) T
Although painful sickle cell crises are increased during pregnancy, they are seen in 27 -50% of women, not over 90%. Blood for all patients with SCD, including pregnant women, should be matched for full CDE and Kell status. Patients with SCD have an increased risk of red cell alloimmunization which is decreased by matching blood using this extended red cell phenotype. Pre-eclampsia and intra-uterine growth restriction are more common in pregnancy women with SCD, and they should be treated as high risk for these complications. Antenatal prophylactic heparin should be administered according to the RCOG Green Top guidelines. Therefore pregnant women with SCD will only be given antenatal thrombo-prophylaxis if they have additional risk factors for thrombo-embolic disease. They should be given thrombo-prophylaxis if they are admitted to hospital in the antenatal period.
8. a) T b) T c) T d) T e) T
These complications are all more common in patients with SCD and should be monitored for before or during pregnancy.
9. a) F b) T c) F d) F e) F
The personal history of thrombosis reveals a provoked event, with a provoking factor that no longer applies. However, there is a strong family history (sister) with an associated heritable thrombophilia, which often causes venous thromboembolism (VTE) in pregnancy (antithrombin); this may apply to this woman. A total of 25–50% of women with a previous VTE have a thrombophilia. An urgent thrombophilia screen should be organised as this may reveal antithrombin deficiency. Although some elements of the thrombophilia screen, such as protein S and lupus anticoagulant may be problematic to interpret in pregnancy, antithrombin is reliable in the absence of acute VTE. Standard thromboprophylaxis and thromboprophylaxis limited to the postpartum would not suffice in a woman with antithrombin deficiency. If the woman is found to be antithrombin deficient, high prophylactic doses should be given in pregnancy and puerperium.
10. a) F b) F c) T d) F e) T
Sudden-onset chest symptoms in pregnant women should not be ignored but investigated. The normal physical examination and chest X-ray do not exclude a pulmonary embolism. Compression ultrasound (CUS) of the legs is a useful test. If a DVT is confirmed, the treatment will be the same as for pulmonary embolism, and further imaging is unnecessary. A negative CUS, however, does not exclude a pulmonary embolism; at least 30% of pulmonary embolisms occur without a detectable DVT. CTPA is the gold standard imaging modality for pulmonary embolism at least outside pregnancy; therefore, this option is correct. It carries a small risk of radiation to the fetus. It is advisable to start anticoagulation with therapeutic doses of LMWH, before and while the definitive investigations are being completed. Prophylactic LMWH is inadequate for treatment purposes. If the chest X ray is normal, the perfusion component of the ventilation–perfusion scan should follow next, even if this is delayed, if available locally. This carries a low risk of radiation to the fetus comparable with that of CTPA.
11. a) F b) F c) T d) T e) F
Anti-Xa levels are not usually necessary to monitor LMWH heparin effect. Heparin has additional effects on the clotting, which may not reflect in anti-Xa levels; therefore, a normal level may not preclude a bleeding complication. The risk of epidural haematoma is small, but if it does occur, it is extremely serious. The 12-h window refers to prophylactic doses. Epidural analgesia is safe given 24 h after the last therapeutic dose. As the DVT was several weeks before and treatment has been given for 7 weeks already, it is safe to withhold one dose of LMWH with ongoing review. If labour does not establish, the dose can be given. Unfractionated heparin is a good alternative: it will cover anticoagulation and can be stopped if the woman starts labour. Provided activated partial thromboplastin time is confirmed normal, epidural is possible 4 h after stopping the UFH infusion. In practice, it is rarely used, as option c is preferred. She may not go into labour and she should not be left without anti-coagulation for a prolonged period.
12. a) F b) T c)T d) T e) F
The woman who has significant risk factors for pulmonary embolism is haemodynamically compromised and with low oxygen saturation, so the suspicion of pulmonary embolism is strong. Thrombolysis should, however, be considered carefully because of the risk of severe bleeding. At this stage, every effort should be made to confirm the suspicion of pulmonary embolism first and exclude internal bleeding as the cause for haemodynamic compromise. In massive pulmonary embolism, the echocardiogram can help by showing impaired right ventricular function because of clot burden. Arterial blood gas will also help in the differential diagnosis. A near normal Hb and significantly low oxygen partial pressure would strengthen the diagnosis of pulmonary embolism. As mentioned above, bleeding should be excluded as the cause of collapse (physical examination of the abdomen, vaginal bleeding, Hb). Unfractionated heparin is the anticoagulant of choice in this case. It reduces clot burden faster than LMWH. In case of an alternative diagnosis, its action can be reversed with protamine sulphate.
13. a) T b) T c) T d) T e) F
The volume of blood transfused and the frequency of transfusion increases the chances of allo-immunisation. In a fetus with ABO blood group compatible with its mother, the risk of allo-immunisation is about 16% in the absence of postnatal anti-D administration. This falls to 1.5–2% if the ABO group is incompatible. This protective effect conferred by the ABO incompatibility is believed to be caused by maternal destruction and subsequent clearance of the ABO-incompatible fetal red-blood cells before rhesus sensitisation can occur. Although the rhesus-D antigen is highly immunogenic, the immune response varies considerably among individuals. Two studies investigating the effect of the volume of fetal blood to which the mother is exposed, reported that as many as 30% of rhesus-D-negative individuals were found not to become allo-immunised even when challenged with large volumes of rhesus-D-positive blood. Parity does not increase the risk of allo-immunisation.
14. a) T b) T c) F d) F e) T
Persistent antibody levels below 4 IU/ml are not associated with severe fetal anaemia. A study by Nicolaides et al. revealed no cases of severe fetal anaemia with antibody levels below 15 IU/L. Antenatal administration of anti-D immunoglobulin at 28 weeks and 34 weeks of gestation to women in their first pregnancies can reduce the risk of immunisation from 1.5%–0.2%. A first affected pregnancy is managed differently to subsequent occasions because the fetal effects of allo-immunisation tend to be less severe first time around, but worsen with each subsequently affected pregnancy. Although some correlation exists between the antibody titre and the severity of disease in a first-affected pregnancy, overall, the level of antibody titre does not predict the severity of disease. In subsequent pregnancies, the most powerful predictor of the severity of disease is the titre at which the fetus was affected previously. Women with a history of an affected pregnancy (e.g. fetal hydrops, intrauterine transfusion, preterm delivery caused by fetal anaemia or neonatal exchange transfusion) are more likely to develop severe fetal anaemia and at an earlier gestation in a subsequent pregnancy. Therefore, they require early assessment for fetal anaemia from about 10 weeks before the gestational age at which the previous pregnancy was affected.
15. a) T b) F c) T d) F e) F
Doppler blood-flow velocity measurement is a useful tool in diagnosing fetal anaemia. Fetal anaemia causes reduced viscosity and increased cardiac output, resulting in an increase of blood-flow velocities in all fetal vessels. Hydrops is not observed until the fetal haemoglobin deficit is at least 7 g/dl below the mean for gestational age, and its development often significantly affects the course of treatment. Doppler assessment of the fetal middle cerebral artery peak systolic velocity has emerged as a suitable tool for predicting fetal anaemia in at risk pregnancies. It is based on the principle that fetal anaemia leads to lowering of viscosity of the blood. The typical fetal heart rate trace usually seen in cases of severe fetal anaemia is a sinusoidal pattern; however, a normal trace does not exclude the presence of fetal anaemia. Haemolysis leads to progressive anaemia in fetuses with rhesus disease. Ultrasound signs of severe fetal anaemia are polyhydramnios, increased placental thickness (over 4 cm), dilatation of the cardiac chambers, increase in the umbilical vein diameter, enlargement of the liver and spleen, and visualisation of both sides of the fetal bowel wall. None of these, however, have proved to be sufficiently reliable for clinical use.
16. a) F b) F c) T d) F e) F
Antibody levels are poorly correlated with the disease severity in non-D allo-immunisation. Management of women with antibodies to other non-rhesus-D, red-cell antigens must recognise the fact that not all of these antibodies are associated with haemolytic disease of the fetus and newborn. Only three antibodies are particularly associated with severe disease: anti-D, anti-c and anti-Kell. With allo-immunisation to the c, E and C antigens, assessment with ultrasound should be considered early because fetal anaemia may occur in these women at levels lower than the recognised critical titre levels for rhesus D antibodies. The use of middle cerebral artery peak systolic velocity to screen for fetal anaemia has been validated and is reliable. It is widely believed that anti-Kell antibodies attack and destroy erythroid precursors, which usually have low haemoglobin levels, ultimately resulting in fetal anaemia without any accompanying increase in bilirubin breakdown products.
17. a) T b) T c) F d) T e) F
APS is associated with intrauterine growth restriction (IUGR). Antiphospholipid antibodies do not solely promote a hypercoagulable state, but trigger an inflammatory response. C4d and C3b fragments are deposited in the placentas of women with APS. Placental insufficiency can develop, as manifested by IUGR. APS is a recognised cause of recurrent miscarriage. It can also cause mid-trimester loss and is associated with pre-term labour; however, the incidence is higher in the first 12 weeks’ gestation. It is estimated that 15% of women who have had recurrent miscarriages are APS positive. No relationship exists between antiphospholipid antibodies and obstetric cholestasis. The pathogenesis of obstetric cholestasis is not clearly understood; however, increased oestrogen and progestogen may play a role as well as a positive family history. Pre-eclampsia is an established risk factor for women with APS. Pregnancy is a hypercoagulable state, and pre-existing thrombophilia can exacerbate this. Infarction and thrombosis of the placenta and decidual vessels can occur, promoting platelet deposition and imbalance of prostaglandins. This in turn can present as pre-eclampsia. APS does not contribute to the development of gestational diabetes. Antiphospholipid antibodies do not influence carbohydrate metabolism or insulin sensitivity.
18. a) F b) F c) F d) T e) T
Recurrent miscarriage is defined as three or more consecutive pregnancy losses. Research studies have defined recurrent miscarriage as two or more consecutive pregnancy losses, possibly due to recruitment issues. The debate on whether recurrent miscarriage should be categorised as two or three pregnancy failures remains ongoing. Recurrent miscarriage occurs in 1% of the general population. Miscarriage will affect about15% of women. Women with high haemoglobin A1c levels in the first trimester are at risk of miscarriage and fetal malformation. Well-controlled diabetes mellitus is not a risk factor for recurrent miscarriage. Most women presenting with recurrent miscarriage are idiopathic. Treatment for women who have experienced recurrent miscarriage has been debated as no pharmaceutical intervention has been proven to improve pregnancy outcome. After three miscarriages, prognosis of a live birth in idiopathic recurrent miscarriage is about 70%. Blood coagulation defects among women who have had recurrent miscarriages have been quoted as high as 60%. Lupus anticoagulant and anticardiolipin antibodies are indicators for APS. Heritable thrombophilia, especially Factor V Leiden and prothrombin gene mutation are indicators for an increased risk of miscarriage.
19. a) F b) T c) F d) T e) T
There is no evidence to suggest heparin improves pregnancy outcome in idiopathic women who have had recurrent miscarriages. Two recently published multi-centre randomised-controlled trials showed no increase in live birth rates with the use of heparin. There is an increased risk of venous thrombosis in pregnancy. This patient has a high chance of developing a further DVT so thrombo-prophylaxis is necessary. Intermediate or even therapeutic doses may be preferred. There is no evidence to suggest that APS is inherited. If her sister were to have an inherited thrombophilia then there would be an argument for carrying out a blood test screen on Patient C. According to guidelines from the Royal College of Obstetrics and Gynaecology and the American College of Obstetrics and Gynecology, heparin in combination with aspirin is the recommended treatment regimen for women who have had recurrent miscarriages who are pregnant with a positive diagnosis of APS. The European Society of Human Reproduction and Embryology advise the use of aspirin, heparin, or both, in the same circumstance. Recent study results have shown the addition of heparin does not influence live birth rate in APS. Current recommendation is to prescribe thrombo-prophylaxis in the 6-week postpartum period for women with a diagnosed inherited or acquired thrombophilia. The risk of a venous thrombosis increases after delivery, and pulmonary embolism remains the leading direct cause of maternal deaths in the UK.
20. a) F b) F c) T d) T e) F
Prednisolone can cause adverse effects on the mother and fetus at any gestation. The risks of hypertension, pre-eclampsia, gestational diabetes, pre-term labour, and osteoporosis are increased, and wound healing is compromised. Previous research suggests that first-trimester exposure is associated with an increased incidence of cleft palate. The suppression of the fetal–hypothalamic–pituitary adrenal axis has also been reported; however, both claims are lacking robust evidence. The recommended daily dose is 75 mg aspirin. Higher doses can promote gastritis, epigastric pain and gastric ulcers. There is no evidence to suggest a higher dose improves pregnancy outcome. In the past, apprehension surrounded the increased risk of osteoporosis as a consequence of prolonged low-dose use of heparin. Pregnancy and lactation adjusts calcium metabolism, and current research has found the use of heparin does not significantly affect this. The activated partial thromboplastin time parameter does not need to be monitored, and low-molecular-weight heparin has fewer reported side-effects. These include bleeding, heparin-induced thrombocytopaenia and osteoporosis. Placebo-controlled trials are needed to either prove or disregard medical treatments for women with thrombophilia who have had recurrent miscarriages.
21. a) T b) F c) F d) F e) F
The sensitivity of cardiothoracic ratio is at least 95%, which is higher than that of placental thickness (77.1%) and MCA PSV (17.6%). Cardiothoracic ratio remains the most sensitive marker in the second trimester for fetal haemoglobin Bart’s disease. Beta-thalassaemia major does not manifest in utero and would not present with anaemic features until after birth. Haemoglobin F (α 2 γ 2 ) is the main type of haemoglobin during fetal life. A beta-thalassaemia carrier has a concomitant alpha trait that will be missed by haemoglobin pattern, as H inclusion bodies can be false–negative.
22. a) T b) T c) F d) F e) T
The absence of a paternal inherited normal beta gene in the maternal plasma indicates that the fetus has not inherited the mutant gene from the father. The presence of paternal inherited normal beta gene in the maternal plasma indicates that the fetus has inherited the normal beta gene from the father instead of the mutant gene. Maternal inherited beta mutant is normally expressed from the mother and hence should be present in maternal plasma. The presence of maternal mutant beta gene in the maternal plasma does not indicate that the fetus has inherited the maternal mutant gene, which is normally expressed from the mother. If the fetus has not inherited any mutant from either the mother or the father, under-representation of the mutant allele is expected and the mutant versus wild-type alleles ratio in the maternal plasma is therefore less than 1.
23. a) F b) T c) T d) T e) F
PGD is feasible for both alpha and beta-thalassaemia. During cleavage-stage biopsy, only one or two cells can be biopsed so that only single-cell polymerase chain reaction can be done. Mono-ICSI reduces the risk of contamination by other sperm DNA. Human leukocyte antigen matching can be done in PGD. Blastocyst biopsy provides more cells for examination.
24. a) T b) F c) F d) T e) F
Von Willebrand disease is the most common inherited bleeding disorder with a prevalence of about 1%. It is not an X-linked disorder. Type 1 and 2 VWD are transmitted as an autosomal dominant trait and type 3 VWD is autosomal recessive in inheritance. Type 1 VWD is the most common, accounting for 70–80% of all women with VWD. It is characterised by a partial deficiency of von Willebrand factor (VWF), and is therefore usually mild. Although carriers of haemophilia have only one affected chromosome, some can have low factor levels resulting from lyonisation. Unlike haemophilia A and B, the correlation between bleeding tendency and factor levels is poor in women with factor XI deficiency.
25. a) F b) T c) F d) F e) T
Hodgkin’s lymphoma is the most common haematological malignancy in pregnancy. Follicular-cell lymphoma is an indolent lymphoma that does not require urgent treatment. Rituximab is a monoclonal antibody against CD20. Both b and e require urgent treatment.
26. a) F b) T c) F d) T e) T
Hodgkin’s lymphoma does not present with disseminated intravascular coagulopathy. This is a classical presentation of acute promyelocytic leukaemia. ABVD is the treatment for Hodgkins lymphoma.
27. a) T b) F c) F d) T e) F
The safety of anagrelide is not established in the first trimester and needs to be stopped. Hydroxycarbamide is not the drug of choice in pregnancy; alpha interferon should be considered in this situation. This woman is considered at high risk of thrombosis and will need both aspirin and low-molecular-weight heparin.
28. a) T b) F c) F d) F e) T
Although medical intervention is often adequate in cases of PPH, the efficacy is lower with massive PPH. In the study by O’Brien et al. haemostasis was achieved with medical treatment in 15% of cases, whereas hydrostatic balloon and the B-Lynch suture arrested bleeding in 75% and 40% of cases. The balloon could be inflated with 200–600 ml of warm sterile water or saline, depending on the size of the uterine cavity. Although incision over the lower uterine segment is not necessary for uterine compression sutures described by Hayman et al. it is needed to apply B-Lynch sutures. Despite various pharmacological agents and introduction of new surgical techniques to control postpartum haemorrhage, some studies have shown no reduction in the prevalence of emergency obstetric hysterectomy. This is likely to be related to the rising caesarean section rates leading to an increasing incidence of placenta accreta. Uterine artery embolisation is most commonly used for elective cases of known placenta accreta. The rapidity of blood loss and logistics of uterine artery embolisation with difficult immediate access to the equipment or an interventional radiologist means that it is less commonly used for emergency PPH.
29. a) F b) T c) T d) F e) F
According to the British Committee for Standards in Haematology’s guidelines, the threshold for blood transfusion is 8 g/dl. The decision to commence blood transfusion should be a clinical decision instead of awaiting the results of full blood count, which invariably leads to delay. The initial haemoglobin value is also not accurate in reflecting the amount of blood loss. Increasing the ratio of clotting products to packed red cells to a ratio of 1:2 or 1:1 fresh frozen plasma: red blood cell ratio during acute obstetric haemorrhage helps to prevent coagulopathy. Recombinant factor VII is not licensed for the treatment of massive postpartum haemorrhage though it is used occasionally. Although tranexamic acid has been shown by reports to reduce the amount of bleeding for postpartum haemorrhage, further research is required before its use can be routinely advocated.
30. a) T b) F c) F d) T e) F
A shock index of greater than 0.9 is associated with a need for intensive therapy on admission. Clinical symptoms and signs of hypovolaemic shock are often delayed because of compensatory mechanisms in these women who are young, fit and healthy. A loss of 1 L of blood requires replacement with 4–5 L of crystalloid (0.9% normal saline or lactated Ringer’s solution) or colloids until cross-matched blood is made available because of the shifting of the intravenous fluid from the intravascular to the interstitial space. Blood loss estimation is commonly underestimated. Royal College of Obstetricians and Gynaecologists suggested that a non-pneumatic antishock garment may be useful in the UK settings where women with PPH require transfer from midwife-led to consultant-led units.
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