Maternal Medical Flashcards
BSL targets for GDM
Fasting 5 or less
1h post- prandial 7.4 or less
2h post- prandial 6.7 or less
Distinguish between Graves flare vs postpartum thyroiditis (with hyperthyroidism)
TSI positive with Graves
Radioactive iodine will show increased uptake with Graves
Diagnosis of AFLP
Swansea criteria: at least 6 of the following:
Hypoglycaemia
Hyperuricaemia
Coagulopathy in the absence of thrombocytopenia
Vomiting
Abdo pain
Diabetes insipidus
Raised ammonia
AKI
raised transaminases
Leucocytosis
Encephalopathy
Diagnosis of Hep B
Screen with Hep B surface antigen- if positive,
Perform Hep B e antigen OR Hep B DNA; + LFTs
Vertical transmission:
95% if both HBsAg + HBeAg +ve
2- 15% if HBsAg +ve but HBeAg -ve
Higher vertical transmission with higher viral load
When to initiate treatment of Hep B and how
If viral load >100 000 000- treat with tenofovir from 30 weeks
Monitor ALT q4weeks, for 2-3 months
Give HBIG + birth dose HBV vaccine to infant
If viral load less than that above, no treatment for mother but give same to infant
Clinical features of TTP
Classic pentad: haemolytic anaemia, thrombocytopenia, fever, neurological manifestations, AKI
Clinical features of HUS
Classic Triad- thrombocytopenia, haemolytic anaemia, renal episode (AKI post- partum usually)
Alpha thalassaemia
4 copies of alpha gene (2 from each parent) which code for alpha globulin chain.
Leads to reduction in synthesis of alpha globulin chains.
3 copies- asymptomatic
2 copies- asymptomatic but May become anaemic in pregnancy
Haemoglobin H (1 copy)- mild- mod anaemia in childhood. In adulthood, can be asymptomatic anaemia to transfusion dependent
Alpha thalassaemia major/ Bart’s hydrops- incompatible with life
Beta thalassaemia
2 copies of beta globulin gene
Trait (one normal gene)- asymptomatic but maybe become anaemic with infection or pregnancy
Major (no normal gene)- lack of beta chain so Hb ends up consisting of an alpha tetramer which results in chronic dysfunction of erythropoiesis ( splenomegaly, infections, long bone deformity, osteoporosis, skull bone expansion, short stature). Patient is transfusion- dependent with endocrine abnormalities
Diagnosis of thalassaemia
Hallmark is very low MCV and MCH.
Consider if normal Hb + above
Offer haemoglobinopathy screening to all women antenatally
Haemoglobin electrophoresis
Screening for thalassaemia
Offer haemoglobinopathy screening to all women antenatally:
- if positive, offer partner screening
- if both partners positive, offer prenatal diagnosis (PCR or southern Blot)
- if affected- involve paeds
Von Willebrand disease (VWD) pathogenesis
vWF is an adhesive protein that has a special role in platelet function and stability of factor VIII.
vWF is required for the binding of platelets to the sub- endothelium after vessel injury.
vWD is a deficiency in vWF
Diagnosis:
- low vWF and factor VIII
- prolonged APTT
3 types:
Type 1- mild
Type 2- qualitative defect
Type 3- severe deficiency
Mx of vWD in pregnancy
Avoid aspirin and NSAIDs (PP)
Type 1- DDAVP IV infusion prior to procedures/ surgery/ regional
Type 2- give FFP prior to procedure
Type 3- FFP prior to procedure
Haemophilia A
X- linked recessive
Low factor VIII levels- improves in pregnancy
Diagnosis:
- prolonged APTT
- low factor VIII levels
Haemophilia B
X- linked recessive
Low factor IX levels
Diagnosis:
- prolonged APTT
- low factor IX levels
Mx of haemophilia A and B
Prenatal:
- confirm genetic status
- genetic counselling- if mum haemophilia carrier, 50% chance of male fetus affected, 50% chance of female fetus carrier
- consider preimplantation genetic testing
- assess effect of DDAVP
Antenatal:
- determine sex of fetus by NIPT (from 10/40)
- CVS at 11-13/40 or amnio from >14/40 to confirm diagnosis
- carrier mothers should have factor levels checked early in pregnancy and again before delivery
- anaesthetic review to discuss regional anaesthesia
Intrapartum:
- IVL- fbc and G&h
- check factor levels before delivery- nvd safe us >40
- treat if <50 and prior to any invasive procedures
— A- DDAVP of factor XIII
— B- TXA or factor IX
- avoid fbs/ fse/ ventouse/ difficult forceps
PP:
- active 3rd stage
- prompt repair of tear
- monitor bleeding
- check + maintain factor levels >40
- contraception advice
- follow- up plan
Neonatal:
- cord blood
- avoid IM injections/ heel pricks until haemophilia status is known
- consider cranial USS if severe neonatal haemophilia
- recombinant factor replacement if bleeding
DIC pathogenesis
Endothelial injury stimulates release of procoagulant substances such as thromboplastin and phospholipid into the circulation, stimulating the coagulation cascade
Increased breakdown/ consumption of coagulation factors and platelets leads to bleeding
Fibrinolysis is stimulated, releasing fibrinogen degradation products (FDPs) which interfere with the production of firm fibrin clots, further exacerbating bleeding
DIC diagnosis
Fibrinogen <2
Low platelet count
Prolonged APTT and PT
Elevated FDPs
Treatment of proximal DVT/ PE in pregnancy
Therapeutic anticoagulation for 6 months or until 6 weeks postpartum (whichever is longer)
Treatment of isolated distal DVT
Therapeutic anticoagulation for 6-8 weeks then prophylactic for the rest of the pregnancy
Risk of child developing epilepsy
4-5% if either parent has it
10% if previously affected sibling
15-20% if both parents have epilepsy
AEDs that are preferred in pregnancy
Leviteracetam
Lamotrigine
Carbamazepine
Major malformations caused by AEDs
NTD
Orofacial clefts
Congenital heart defects
Pathogenesis of CF
Autosomal recessive
Caused by abnormalities in the CF transmembrane conductance regulator protein (CFTR gene) responsible for sodium chloride channels, causing impaired movement of water and electrolytes across epithelial surfaces,
This leads to exocrine gland dysfunction, with thick mucous and increased sweat sodium
