1705801
Description
Flashcards by Anna Walker, updated more than 1 year ago
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Created by Anna Walker
over 9 years ago
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| Question | Answer |
| How does an ECG change during pregnancy? | There is a left axis shift and inverted T waves are common. 90% of women have a flow (ejection systolic) murmur due to increased blood flow. |
| What are the principles of managing cardiovascular disease in pregnancy? | Pts with severe disease preferably assessed before pregnancy. Some drugs such as warfarin and ACEIs are contraindicated in pregnancy. Those with severe decompensated disease are advised against pregnancy. Cardiac assessment, esp echo, is needed. HTN should be treated. Women who have conceived on contraindicated drugs will need to have these altered: care needs to be individual but beta blockers are often used for HTN. Thromboprophylaxis needs to be continued, but usually with a LMWH. Regular checks for anaemia are made. In labour, attention is paid to fluid balance; elective epidural analgesia reduces afterload. Elective forceps delivery helps avoid the stress of pushing in severe cases. Antibiotics in labour are recommended for some (e.g. if replacement valves to protect against endocarditis. |
| Name some mild cardiac abnormalities that may not need managing in pregnancy. | Mitral valve prolapse, patent ductus arteriosus, VSD or ASD. |
| On what occasion may warfarin be used in pregnancy? | Artificial metal valves are particularly prone to thrombosis and warfarin is used after the first 12 weeks, despite its fetal risks. |
| What is peripartum cardiomyopathy? What are the potential complications? What is the treatment? | This is a rare (1 in 3000) cause of heart failure, specific to pregnancy. It develops in the last month or first 6 months after pregnancy and in the absence of an identifiable cause. It is frequently diagnosed late. It is a cause of maternal death (risk 15%) and in more than 50% of cases leads to permanent left ventricular dysfunction. Treatment is supportive, with diuretics and ACEIs. There is a significant recurrence rate in further pregnancies. |
| What effects might pregnancy have on respiratory disease? | Tidal volume increases by 40% in pregnancy, although there is no change in respiratory rate. Asthma is common in pregnancy. Pregnancy has a variable effect on the disease: drugs should not be withheld, because they are generally safe and because a severe asthma attack is potentially lethal to mother and fetus. Well-controlled asthma has little detrimental effect on perinatal outcome. Women on long-term steroids require an increased dose in labour because the chronically suppressed adrenal cortex in unable to produce adequate steroids for the stress of labour. |
| What effects might pregnancy have on epilepsy? | Affects 0.5% of pregnant women. Seizure control can deteriorate in pregnancy. and particularly in labour. It is a significant cause of maternal death and antiepileptic treatment is continued. However, the risk of congenital abnormalities (e.g. NTDs) is increased (4% overall) and this is largely due to drug therapy. The risks are dose-dependent, higher with multiple drug ise and higher with certain drugs (e.g. sodium valproate). The newborn will have a 3% risk of developing epilepsy. |
| What would you do in a pre-conceptual assessment of a woman with epilepsy? | Aim for seizure control with as few drugs as possible at the lowest dose, together with folic acid (5mg/day) supplementation. Ideally, sodium valproate should be avoided as it is associated with a higher rate of congenital abnormalities and lower intelligence in children. However, preconceptual advice is rarely sought and fear of recurrence of seizures and losing the driving licence often prevent drug changes. Therefore, all women aof reproductive age are best managed as if they are contemplating pregnancy. Carbamazepine and lamotrigine are safest. In women without complete seizure control, doses may need to be increased, but the benefits of routine drug level monitoring remain debated. Folic acid is continued throughout pregnancy and from 36 weeks, 10mg vit K is given orally as the epilepsy medication can cause fetal haemorrhage. The 20 week scan and fetal echo are important to exclude fetal abnormalities. |
| What are the changes in the thyroid in pregnancy? | Thyroid ststus doesn't alter in pregnancy, though iodine clearance is increased. Goitre is more common. Fetal thyroxine production starts at 12 weeks, before this, it is dependent on maternal thyroxine. Maternal TSH is increased in early pregnancy. |
| How might hypothyroidism affect a pregnancy? | This affects 1% of pregnanct women. In the UK, most cases of hypothyroidism are due to Hashimoto's thyroiditis or thyroid surgery, but hypothyroidism is common where dietary iodine is deficient. Untreated disease is rare as anovulation is usual, but it is associated with with a high perinatal mortality. Even subclinical hypothyroidism is associated with miscarriage, prematurity and intellectual impairment in children. Hypothyroidism is also associated with a slightly increased risk of pre-eclampsia, particularly if antithyroid antibodies are present. Replacement with thyroxine is important and TSH levels are monitored 6-weekly: in normal pregnancy the TSH is lowered overall, so the dose may need to be increased until delivery. |
| How might hyperthyroidism affect a pregnancy? | Affects 0.2% of pregnant women and is usually due to Grave's disease. Untreated disease rare in pregnancy as anovulation is usual. Inadequately treated disease increases perinatal mortality. Antithyroid antibodies can cross the placenta - rarely this causes neonatal toxicosis and goitre. For the mother, toxicosis may improve in late pregnancy but poorly controlled disease risks a 'thyroid storm' whereby the mother gets acute symptoms and heart failure, usually near or at delivery. Symptoms may be confused with those of pregnancy. Hyperthyroidism is treated with propylthiouracil (PTU) rather than carbimazole. PTU crosses the placenta and can occasionally cause neonatal hypothyroidism: the lowest possible dose is used and thyroid fundtion is monitored monthly. Grave's disease often worsens postpartum. |
| What is postpartum thyroiditis? | This is common (5-10%) and can cause postnatal depression. Risk factors include antithyroid antibodies and type 1 diabetes. In affected patients, there is a transient and usually subclinical hyperthyroidism, usually about 3 months postpartum, followed after about 4 months by hypothyroidism. This is permanent in 20%. |
| What is acute fatty liver? | This is a very rare (1 in 9000) condition that may be part of the PET spectrum. Acute hepatorenal failure, DIC and hypoglycaemia lead to a high maternal and fetal mortality. There is extensive fatty change in the liver. Malaise, vomiting, jaundice and vague epigastric pain are early features, while thirst may occur weeks earlier. Early diagnosis and prompt delivery are essential, although correction of clotting defects and hypoglycaemia are needed first. Treatment is then supportive, with further dextrose, blood products, careful fluid balance and, occasionally dialysis. The recurrence rate is low. |
| What is Antiphospholipid syndrome (APS)? | This is when the lupus anticoagulant and/or anticardiolipin antibodies (ACA) occur (measured on at least 2 occasions at least 3 months apart) in association with adverse pregnancy complications. Because of placental thrombosis, recurrent miscarriage, IUGR and early pre-eclampsia are common, and the fetal loss rate is high. Low levels of these antibodies are also present in nearly 2% of all pregnant women and therefore treatment, usually with aspirin and LMWH is restricted to those with the syndrome. The pregnancy is managed as 'high risk', with serial USS and elective induction of labour at least by term. Postnatal anticoagulation is recommended to prevent venous thromboembolism. |
| What is the management of a women with a prothrombotic condition in pregnancy? | E.g. antithrombin deficiency, protein C and S deficiency, factor V Leiden heterozygosity (to a lesser extent). Treatment is usually with high-dose folic acid. Women with prothrombotic tendencies and an adverse pregnancy history are usually treated as for APS, although effectiveness of this is unproven. Postnatal anticoagulation is recommended. |
| What happens to the urea and creatinine levels in pregnancy? | GFR increases 40%, causing the urea and creatinine levels to decrease. |
| How might chronic renal disease affect a pregnancy? | Affects 0.2% of pregnant women. Fetal and maternal complications depend upon the degree of HTN and renal impairment. Pregnancy is inadvisable if the creatinine is >200mmol/L. Renal function often deteriorates late in the pregnancy: this is more common in severe disease and can lead to permanent deterioration. Rejection of renal transplants is not more common; immunosuppressive therapy, e.g. ciclosporin, must continue. Proteinuria can cause diagnostic confusion with PET, which is more common, but it will usually have been present before 20 weeks. Fetal complications include PET, IUGR, polyhydramnios and preterm delivery. Management involves USS for fetal growth, measurement of renal function, screening for urinary infection (which may exacerbate renal disease) and control of HTN. In severe cases dialysis is indicated. Vaginal delivery is usually appropriate. |
| What are the risks of a UTI in pregnancy? | Urinary infection is associated with preterm labour, anaemia and increased perinatal morbidity and mortality. Asymptomatic bacteriuria affects 5% of women, but in pregnancy is more likely (20%) to lead to pyelonephritis. The urine should be cultured at the booking visit and asymptomatic bacteriuria is treated. Subsequently, culture is performed if nitrites are detected on routine urinalysis. Pyelonephritis affects 1-2% of women, causing loin pain, rigors, vomiting and a fever. This requires treatment with IV Abx. E coli accounts for 75% and is often resistant to amoxicillin. |
| What happens to the risk of VTE in pregnancy? | Pregnancy is prothrombotic and the incidence of VTE is increased six-fold, witht the risk is highest in the postnatal period. Blood clotting factors are increased, fibrinolytic activity is reduced and blood flow is altered by mechanical obstruction and immobility. Women with inherited prothrombotic conditions and those with a family or personal Hx are particularly prone to thromboses. |
| Describe the risks of PE in pregnancy. | PE is an important cause of maternal death in developed countries; in the UK it has become less common because of better thromboprophylaxis. Embolism occurs in <0.3%, with a mortality of 3.5%. Diagnosis is as in the non-pregnant woman using a CXR, arterial blood gas analysis, and CT or with perfusion+/- ventilation (VQ) scanning. The ECG changes of normal pregnancy can imitate a PE. |
| Describe the risks of DVT in pregnancy. | Occurs in about 1% of pregnant women. Thromboses are more often iliofemoral and on the left. Doppler examination and occasionally a venogram are used. |
| What is the management of DVT/PE in pregnancy? | Clinical signs of both a PE and a DVT may be absent; the former may only be diagnosed at postmortem. A thrombophilia screen is performed before treatment. VTE is treated with subcut LMWH. Doses are adjusted according to the anti-factor Xa level: more is needed than in non-pregnant women as clearance is more rapid. If possible, treatment is stopped shortly before labour, but is restarted and continued into the puerperium, Warfarin is teratogenic, may cause fetal bleeding and is seldom used antenatally. |
| How is thromboprophylaxis used in pregnancy? | Thromboprophylaxis should be used frequently because of the importance of PE as a cause of maternal death. Every woman rquires an early antenatal 'risk assessment' which is reviewed according to subsequent events, such as C/S or hospitalisation. Algorithms are complex. COMPRESSION STOCKINGS are useful for when LMWH is contraindicated (eg during/postsurgery)/ Antenatal prophylaxis with LMWH is restricted to women at very high risk, such as previous thrombosis, particularly if unprovoked/with a thrombophila, or those hospitalised/immobile and with other risk factors, maternal weight determines dosage. Postpartum prophylaxis with LMWH is frequently used, and according to individual risk assessment. If there are two or more moderate risk factors, or one intermediate risk, LMWH is prescribed for at least a week. LMWH can usually be given by 24h after C/S or NVD. Clexane (enoxaparin) usually used. |
| What are the risks in pregnancy associated with obesity? | MATERNAL: obese women have a higher risk of thromboembolism, PET and DM, C/S, wound infections, difficult surgery, PPH and maternal death. FETAL: A higher rate of congenital abnormalities (eg NTDs), DM and PET means that perinatal mortality is increased two- to three-fold. |
| How is obesity managed in pregnancy? | Preconceptual weight advice is ideal; high dose (5mg) preconceptual folic acid supplementation is recommended. Vit D is recommended. Weight is best maintained: loss in pregnancy is impractical and likely to cause malnutrition. The pregnancy should be considered igh-risk, particularly if the BMI is 35 or more. Screening for GDM and closer blood pressure surveillance with an appropriately sized cuff are required. A formal anaesthetic risk assessment is recommended if BMI is 40 or more. Thromboprophylaxis is frequently used. There is an increasing and probably undesirable trend towards ELSCS in very obese women. |
| What are the effects of pregnancy on a woman with HIV? | Pregnancy does not hasten progression to AIDS ('severe HIV'). The incidence of PET is greater in HIV infected women, and this may be increased by antiretroviral therapy. GDM may also be more common. |
| What are the effects of maternal HIV on a fetus/neonate? | Stillbirth, PET, IUGR and prematurity are more common. Congenital abnormalities are not, ant antiretrovirals are not teratogenic, but folic acid antagonists (e.g. co-trimoxazole) are often prescribed to HIV infected women. The most important risk is of vertical transmission. This is mostlyu beyond 36 weeks, intrapartum or during breastfeeding. It occurs in 15% in the absence of preventative measures, and in up to 40% of breastfeeding women in Africa, although passively acquired antibodies in the neonate are universal because of transplacental transfer. Transmission is greater with low CD4 counts and a high viral load (early and late-stage disease), co-existent infection, premature delivery and during labour, particularly with ruptured membranes for more than 4h. 25% of HIV infected neonates develop AIDs by 1 year and 40% will develop AIDS by 5 years. |
| What is the management of pregnant women with HIV? | WOmen should be managed in conjunction with a physician and have regular CD4 and viral load counts. Prophylaxis against PCP is given if the CD4 count is low. Drug toxicity is monitored with liver and renal function. Hb and blood glucose testing. Genital tract infections such as Chlamydia should be sought. The ideal policy to prevent vertical transmission is highly active antiretroviral therapy (HAART), currently including zidovudine, which reduces viraemia and maternal disease progression. This is continued throughout pregnancy and delivery, and the neonate is treated for the first 6 weeks. If women are not already on the therapy, it is usually started at around 28 weeks. C/S is performed and breastfeeding is avoided. This strategy reduces vertical transmisssion to <1%. |
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