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22 Cards in this Set

  • Front
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Describe the pathophysiology of gestational DM
Occurs around 24-28 wks GA, anti-insulin factors (human placental lactogen, progesteron, hCG, cortisol)produced by placenta and high maternal cortisol levels created increased peripheral insulin resistance --> higher fasting glucose --> GDM and/or exacerbating pre-existing DM
RF for gestational DM
> 25
obesity
family history
previous history
from diabetes prone ethnic group
previous child with birthweight > 4kg
fetal macrosmia
persistant glycosuria
When should woman be screened for gestational DM
24-28 wks GA
How should woman be screened for gestaional DM
At 24-28 weeks
Oral glucose challenge test - Pt drinks 50g glucose drink - 1hr later - BSL
PG should be < 7.8 if > 10.3 = GDM no need for GTT
PG 7.8 - 10.3 - do 2 hr 75g OGTT
OGTT - 150mg carb loading 3 days prior; Fast 14 hrs; Measure BSL; Drink glucose; test every hour for 3 hours
FG > 5.3; 1 hr > 10.6, 2 hrs > 8.9 -->
2/3 = GDM
1/3 = impaired glucose tolerance
Management of diabetes in pregnancy
Diet management = first line
if blood glucose not well controlled - insulin or if developing fetal macrosomia

Maintain normal blood glucose levels, take folic acid, have good diet, preferably change to insulin therapy if on hypoglycaemia agents
What is an HBA1c value > 140% of pre pregnancy value associated with?
Risk of spontaneous abortions and congenital malformation
What fetal complications are associated with DM in pregnancy
Growth abnormalities: macrosomia; IUGR
Delayed lung maturity (hyperglycaemia interferes with surfactant synthesis)
Congenital anomalies (DM1 and 2 NOT GDM b/e develops after critical period of organogensis)
Preterm labour/prematurity, stillbirth, birth trauma
Neonatal hypoglycaemia, hyperbilirubinaemia and jaundice, hypocalcaemia, polycythemia (hyperglycaemia stimulates fetal EPO production)
Maternal complications of DM in pregnancy
Hypertension/pre-eclampsia
Polyhydramnios
Hypoglycaemia, ketoacidosis, diabetic coma
End-organ involvement or deterioration (not GDM retinopathy, nephropathy)
Pyelonephritis
Increased incidence of spontanous abortion (DM1 and 2 not GDM) - related to pre-conception glycaemic control
What is the risk of GDM mothers developing type 2 diabetes?
2 different stats
4x10 risk
50% risk in the next 20 years
Can oral hypoglycaemics be used in pregnancy?
NO - safety has not been established
Should mums with DM have a C/S
if diet controlled - can progress naturally
If insulin - induce at 39 weeks
or if EFW > 4.5kg
What is cholestatic jaundice of pregnancy
clinical syndrome characterised by intense pruritus that precedes jaundice by 7-14 days
Clinical features of cholestatic jaundice in pregnancy
intense pruritus (classically worst on palms and soles of feet) +/- icterus 1-2 weeks later
ALT < 500 IU, ALP, GGT markedly elevated
Steatorrhea unusual
What are the complications with cholestatic jaundice in pregnancy?
Can cause reduced Vit K absorption --> PPH
Increased risk of prematurity, foetal distress, and foetal loss
At what stage GA is cholestatic jaundice in pregnancy typically seen?
17-29 weeks
How do you manage cholestatic jaundice in pregnancy?
manage itch with cholestyramine
Prophylactic Vit K before delivery
Ursodeoxycholic acid daily
What is acute fatty liver of pregnancy?
Form of hepatic failure with coagulopathy and encephalopathy that is characterised by microvesicular fatty infiltrates in liver parenchyma
Pathogenisis unknown
When does acute fatty liver of pregnancy usually occur?
3rd trimester (28-40 weeks GA)
Resolution of hepatic function with delivery or termination of pregnancy
Risk factors for acute fatty liver of pregnancy
Primigravidas
Male gestation
Long chain acyl-CoA dehydrogenase deficiency with at least one allele for the G1528 mutation in either mother or fetus
NO recurrence with subsequent pregnancies
Clinical features of acute fatty liver of pregnancy
acute N/V, severe upper abdominal pain preceding jaundice
confusion
pre-eclampsia
pruritus
range in presentation mild - fulminant: GI bleeding, hepatic coma, renal failure, true hepatic failure (coagulopathy and encephalopathy)
How do you diagnose acute fatty liver of pregnancy?
Elevated PTT and low serum fibrinogen
AST>ALT
hypoglycaemia
Pre-eclampsia and HELLP
liver biopsy to establish diagnosis
US/MRI/CT not consistently useful in confirming AFLT but if liver biopsy is not impossible CT is more helpful in showing a reduced attentuation of the liver that is compatible with AFLP
Management of acute fatty liver of pregnancy?
early diagnosis with prompt delivery followed by maxiamal supportive care