DM and thyroid in pregnancy Flashcards
Endocrine metabolic changes in pregnancy
Early in gestation- anabolic state
Later in gestation- increased basal and post-prandial glucose (increased insulin release beta cell hyperplasia, fasting AM hypoglycemia)
Increased insulin resistance (decreased cellular glucose uptake and response 50-60% increase in resistance)
Increased lipids and triglycerides (increased lipid metabolism, hyperketonemia)
the goal is to supply glucose to grow fetus
hPL (human placental lactinogen )
Produced by trophoblast, highest in the 3rd Trim
Functions:
Decreases insulin sensitivity (increases insulin resistance)
Decreases maternal glucose uptake and utilization
Anti insulin/prodiabetogenic
Placental transport of nutrient
Amino acid transport via active transport
glucose transport vi Facilitated diffusion
Fatty acids via placental metabolism
Placental glucose transport
GLUT 1 is the principal glucose transporter, located in the syntiotrophoblase via facilitated diffusion
Gestational Diabetes mellitus
Definition- Onset of abnormal glucose tolerance during pregnancy
Risk factors- obesity, previous pregnancy affected by GDM, family history of DM, Af Am, hispanic or asian ethnicity
Physiologic changes with GDM- Peripheral insulin resistance (Beta cell hyperplasia, beta cells secrete more insulin, insufficient response–> diabetes)
Maternal hyperglycemia- (lead to a maternal hyperinsulinia as a feedback, fetal hyperglycemia (fetal hyperinsulinemia
GDM complications
Fetal complications- macrosomia, polyhydramnios, neonatal hypoglycemia, polycythemia, hypocalcemia, hypomagnesium, birth trauma (shoulder dystocia), respiratory distress, long term risk of metabolic disorder/diabetes
Maternal- injury, c-section, preeclampsia, future T2DM
Management- diet, exercise, glycemic control
Screening and management GDM
Screen all women at 24-28 weeks, 1 hour glucose load (>140) , comfirm with 3 hr glucose load (>90)
A1GDM- diet control
A2GDM- controlled with medictaions (insulin, metformin, glybride)
Post partum 6 weeks 2 hour glucose test
Macrosomia
> 4kg, abnormal fat distribbution,
Can lead to shoulder dystocia, C-section, 3rd and 4th degree laceration
Baby will be hypoglycemic after birth because in a hyperinsulinemic state
Thyroid changes in pregnancy
hCG stimulates TSH receptor - share the alpha subunit
Increased thyroxine-binding globulin (TBG), increased bound t3 and t4
Placenta transfer- TSH does not cross placenta, T4 can cross the placenta
Fetal thyroid gland begins functioning at 20 weeks
Hypothyroidism in pregnancy
Elevated TSH, decreased f T4
Causes-
Iodine deficiency- most common cause world wide of hypothyroidism, higher dietary requirement during pregnancy (increased TBG, increased TH production, renal iodine excretion, fetal iodine need)
Associated with goiter, neurocognitive deficits
Hashimotos thyroidits (Autoimmune)
hashimotos thyroiditis
most likely cause in Us, lymphocytic infiltration of thyroid gland (leads to goiter or atrophy), presence of thyroid peroxidase autoantibodies (antiTPO), TBG (autoantibodies anti TBG)
Increased risk of miscarriage, preterm delivery, fetal neurocognitive problems, pre-eclampsia, abruption, low birth weight
Treatment- levothyroxine
Hyperthyroidism in pregnancy
Low TSH elevated fT4
Symptoms- goiter, ophthalmopathy, tachycardia, muscle weakness, tremor
Risks, SAB, preterm labor, IUFD, low birth weight, pre eclampsia, heart failure
Causes: graves disease, hCG mediated hyperthyroidism
Graves disease
Circulating thyroid stimulating IgG autoantibodies
Can cross the placenta and lead to fetal thyroid dysfunction (still present even after surgiccal or radioactive ablation of the thyroid- mothers will be hypothyroid but possess the antibodies
Gestational thyrotoxicosis hCG ( is worst in the 1st trimester, molar pregancny), really bad emesis
Hyperthyroidism treatment- thiomides
Propylthiouracil (PTU)- inhibits conversion of t4 to t3, limited ability to cress placenta, maternal hepatitis, avoid long term and only give in 1t
Methimazole- inhibits synthesis of t3 and t4 in thyroid, Se- embryopathy- esophageat atresia, aplasia aovid in T 1
