Maternal Medical Flashcards

1
Q

BSL targets for GDM

A

Fasting 5 or less
1h post- prandial 7.4 or less
2h post- prandial 6.7 or less

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2
Q

Distinguish between Graves flare vs postpartum thyroiditis (with hyperthyroidism)

A

TSI positive with Graves
Radioactive iodine will show increased uptake with Graves

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3
Q

Diagnosis of AFLP

A

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

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4
Q

Diagnosis of Hep B

A

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

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5
Q

When to initiate treatment of Hep B and how

A

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

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6
Q

Clinical features of TTP

A

Classic pentad: haemolytic anaemia, thrombocytopenia, fever, neurological manifestations, AKI

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7
Q

Clinical features of HUS

A

Classic Triad- thrombocytopenia, haemolytic anaemia, renal episode (AKI post- partum usually)

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8
Q

Alpha thalassaemia

A

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

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9
Q

Beta thalassaemia

A

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

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10
Q

Diagnosis of thalassaemia

A

Hallmark is very low MCV and MCH.
Consider if normal Hb + above

Offer haemoglobinopathy screening to all women antenatally
Haemoglobin electrophoresis

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11
Q

Screening for thalassaemia

A

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

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12
Q

Von Willebrand disease (VWD) pathogenesis

A

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

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13
Q

Mx of vWD in pregnancy

A

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

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14
Q

Haemophilia A

A

X- linked recessive
Low factor VIII levels- improves in pregnancy
Diagnosis:
- prolonged APTT
- low factor VIII levels

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15
Q

Haemophilia B

A

X- linked recessive
Low factor IX levels
Diagnosis:
- prolonged APTT
- low factor IX levels

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16
Q

Mx of haemophilia A and B

A

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

17
Q

DIC pathogenesis

A

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

18
Q

DIC diagnosis

A

Fibrinogen <2
Low platelet count
Prolonged APTT and PT
Elevated FDPs

19
Q

Treatment of proximal DVT/ PE in pregnancy

A

Therapeutic anticoagulation for 6 months or until 6 weeks postpartum (whichever is longer)

20
Q

Treatment of isolated distal DVT

A

Therapeutic anticoagulation for 6-8 weeks then prophylactic for the rest of the pregnancy

21
Q

Risk of child developing epilepsy

A

4-5% if either parent has it
10% if previously affected sibling
15-20% if both parents have epilepsy

22
Q

AEDs that are preferred in pregnancy

A

Leviteracetam
Lamotrigine
Carbamazepine

23
Q

Major malformations caused by AEDs

A

NTD
Orofacial clefts
Congenital heart defects

24
Q

Pathogenesis of CF

A

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

25
Q

Pre- pregnancy management on woman with CF

A

Counselling
Pregnancy contraindicated if pulmonary HTN, Cor pulmonale or FEV1 <30-40% predicted.
Assess risk of affected child:
- mum always homozygous
- if partner status unknown, based on background carrier risk 1:25- chance is 2- 2.5%
- 50% if father heterozygous for all gene
- offer amnio/ CVS once pregnant OR
- offer:
— artificial insemination with donor sperm
— donor egg + partners sperm
— preimplantation genetic testing

Optimise maternal condition
- nutrition- check diabetes, pancreatic enzymes, high calorie supplements
- cardiopulmonary status

26
Q

Pregnancy complications of influenza infection

A

Fetal:
- spont miscarriage
- low birthweight
- PTB
- if infection in first trimester- increased risk of hydrocephaly, cleft lip, NTD, congenital heart defects

27
Q

Why do we vaccinate mums against influenza in pregnancy

A

Protects the infant for the first 6 months of life with a 60% reduction in influenza

28
Q

Pathogenesis of coronavirus

A

Single- stranded enveloped RNA virus

Infects type 2 alveoli via ACE- 2 and its membrane- bound receptor

29
Q

Uteritonics to use with caution in asthmatic mum

A

Carboprost
Ergometrine
?miso

30
Q

Effects of overt hypothyroidism on pregnancy- maternal

A

Subfertility
Miscarriage
Pre- eclampsia/ abruption
Anaemia
Postpartum depression

31
Q

Effects of hypothyroidism on pregnancy- fetal

A

Growth restriction/ low birthweight
Stillbirth
Reduced IQ/ neuro developmental delay
Permanent brain damage/ cretinism

32
Q

Features of renal graft rejection

A

Worsening Cr
Fever
Oliguria
Graft swelling and tenderness
Altered echogenicity of renal parenchyma and blurring or corticomedullary junction on USS

Definitive diagnosis is renal biopsy