Diabetic Embryopathy: Pathophysiology and Fetal Malformations
Terms in this set (33)
infants of diabetic mothers
Pathophysiology insulin production
Levels of estrogen and progesterone rise throughout pregnancy, these hormones affect glucose homeostasis increasing tissue insulin-resistance, there is a compensatory effort by the pancreatic beta-cells to produce more insulin causing 30% increase in maternal insulin needs as pregnancy progresses.
Pathophysiology - insulin effects
Insulin stimulates glycogen deposition and decreases hepatic glucose production. Insulin also increases protein and fatty acid production and storage known as "the fed state"
Pathophysiology: insulin, glucose, and diabetes
Maternal glucose crosses placenta membrane but insulin does not so fetal levels are maintained at 20-30 mg/dl less. Inadequate maternal pancreatic insulin response results in maternal &fetal hyperglycemia. Surging maternal and fetal glucose levels are accompanied by episodic fetal hyperinsulinemia.
Pathophysiology: cascading effects
Fetal hyperinsulinemia promotes excess nutrient storage resulting in macrosomia, fetal oxygen levels deplete result in hypoxia and then surges in adrenal catecholamine levels cause hypertension leading to cardiac remodeling and hypertrophy.
Cascading effects of hypoxia
production of erythropoietin thereby increasing red cell mass. High hematocrit values in the neonate leads to vascular sludging, poor circulation, and postnatal hyperbilirubinemia.
glycosylated hemoglobin 'HbA1C' indicates glucose levels in fetus, frequency of congenital anomalies in patients with normal or high 1st trimester glycohemoglobin HbA1C >8.5 values was 3.4%. poor glycemic control in periconceptions period HbA1C> 8.5 had a 22.4% rate of malformation
Cardiovascular malformations in 3-9%, Anencephaly 13-20x increased risk, flexion contractures of limbs, vertebral anomalies, cleft palate, intestinal anomalies e.g. small colon syndrome, caudal regression syndrome i.e. sacral lumbar anomalies 200x more frequently than general population.
VSD, TOF, truncus arteriosus, transposition of the great arteries, aortic stenosis/coarction of the aorta, tricuspid atresia, atrial septal defect, single umbilical artery, hypoplastic left heart, double outlet right ventricle, PDA.
Congenital heart defects
some show abnormal cell migration i.e. supracristal ventricular septal defects, TOF, TA. Some abnormal response to cell signalling e.g. PDA, valvular anomalies. Abnormalities in the TGF beta signaling.
hypertrophic cardiomyopathy occurs in ~30%, asymmetric septal hypertrophy, 5-10% have poor cardiac output, respiratory distress, or heart failure, death is rare. Most resolve in 6 moths with therapy. Thought to be due to hyperinsulinemia.
16 times more likely: 13x for anencephaly, 20x for spina bifida, 200x caudal dysplasia, microcephaly, holoprosencephaly. Maternal obesity a possible contributing factor.
Ear anomalies, renal anomalies i.e. rena agenesis and renal dysplasia, gastrointestinal i.e. duodenal atresia, anorectal atresia, small left colon syndrome.
Thymus hypoplasia, parathyroid hypoplasia, conotruncal heart defects.
caudal regression i.e. sirenomelia, sacral dysgenesis, segmentation disorders
Femoral Hypoplasia unusual facies
cleft lip with/without cleft palate, cleft palate, Pierre Robin sequence
seen in up to 20% of pregnancies complicated by diabetes, most often associated with maternal GDM of longer duration with complications i.e. renal disease, hypertension, poor glycemic control.
70% of neonatal macrosomia due to constitutional and gestational factors
Fetal macrosomia early gestational complications
fetal macrosomia late gestation complications
fetal macrosomia delivery complications
Perinatal Morbidity in diabetic pregnancy
IDM hypoglycemia managments
IDM respiratory distress 1
IDM respiratory distress 2
IDM polycythemia and hyperviscosity syndrome
complications of polycythemia
Long-term risks to IDMS: neurocognitive outcome
Long-term risk: obesity
Prevention of fetal malformations
Management of pregnancy for diabetics
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