Medical Complications of Pregnancy Flashcards
Changes in insulin requirements for Type 1 diabetics during pregnancy
Changes in glucose metabolism early (1st trimester); Anabolic state
- Increase in maternal fat stores
- Decrease in free fatty acids
- Decreased insulin requirements
Late: Diabetogenic state
- Increased insulin requirements
- Decreased fasting glucose
- Decreased insulin sensitivity
Glucose toxicity to fetus
- Too much glucose is toxic to fetus
- Organogenesis is complete by 9wks
*insult through glucose can occur 6-9wks gestation
- Placenta has GLUT transportes for facilitated glucose transport
- Preconception counseling is key to prevention of birth defects
Important time periods during pregnancy
- <5wks: miscarriage
*fetus is just beginning to develop; if theres insult at this period of time the fetus will be aborted
- 6-10wks (problem period): Organogenesis
*birth defects can occur during this period so important to control for medications/drug use
- 10-20wks: out of the danger zone
*can potentially put women back on their meds at this time if they really need it
- >20wks: growth tissues, preterm labor
*can’t cause birth defects at this point but can cause growth issues as this is where the fetus is just growing
HbA1c value vs risk of major malformation
- HbA1c correlates very closely to birth defects
- The goal for diabetic mothers is <6
*some women especially Type 1 diabetics cannot reach this level so aim for 6-6.5mg/dL
- 2 main areas that result in defects in diabetic babies are the heart and the brain
Fetal complications of diabetics mothers
- Macrosomia (birth weight >9lbs)
*carries a high risk of birth injury; shoulder dystocia, brachial plexus injury
- Miscarriage
- Neonatal complications
*respiratory distress
*jaundice
*hypoglycemia
Maternal complications with diabetes
- Preeclampsia
*90% preeclampsia
*almost 100% premature, average 34wks
*20% stillbirths
- Ketoacidosis
- Worsening end-organ dmg
*nephropathy; kidney dmg reduced w/ ACE inhibitors
*retinopathy (2x rate of progression)
*CAD (increased risk of MI, especially in 3rd trimester (28wks)
- Much more likely in Type 1 to have these issues
ACE inhibitors during pregnancy
- Cause birth defects
- Increased heart defect
- Can cause permanent renal dmg, oligohydramnios
- Fetuses w/ renal dysplasia are typically not compatible w/ life
Medication regimen for diabetics during pregnancy
- Switch from oral meds to insulin
- Stop ACEI, ARBs
Maternal thyroid physiology during pregnancy
- Increased TBG (due to estrogen)
*more of the thyroxine becomes bound up in these proteins and less is free stimulating the thyroid to produce more thyroxine
- Placenta can de-ionize thyroxine also causing an increase in thyroid production
*causes increase thyroxine production
- Increase in iodine clearance (increased GFR)
*increased iodine requirement during pregnancy
- BhCG mimics TSH
*decreased TSH—>increase T4 (neg feedback)
Thyroid hormones to monitor during pregnancy
- Want to check the free ones
- Free T3 and T4 are the only ones you want to watch during pregnancy
Fetal thryoid development
- Fetal thyroid develops ~9wks
- Produces thyroid hormone by 18wks
*less than 18wks the fetus is completely dependent on mother for thyroxine
*starts uptaking iodine by 10-14wks
- Relies on maternal thyroid hormone until mid-2nd trimester
hCG effect on thyroid
- Can have a transient effect in increasing thyroid function by mimicing TSH resulting in lower levels of TSH
- Can mimic a hyperthyroidism
Iodine deficiency in fetus
- Leading cause of preventable mental retardation
- Mean IQ loss of 13 points
- 1920’s, table salt iodinated
*20% increase in IQ
- Not as big of an issue in the US but worldwide
Thyroid function across placenta
- Thyroid antibodies can cross the placenta which are a big issue with autoimmune thyroid diseases (particularly Grave’s)
*predominantly thyroid stimulating antibodies
*can have thyroid blocking antibodies
*thyroid peroxidase antibodies (Hashimoto’s)
- Most of the effect is going to be from the thyroid stimulating antibodies
- Maternal TSH does not cross the placenta so will be no neg. feedback from mother
Fetal complications of hyperthyroidism
- Growth restriction
- Prematurity
- Stillbirth
- Miscarriage
- Tachycardia
- Goiter
- Preeclampsia
Maternal Graves Disease Medication options
- Women w/ grave should be treated medically or undergo ablation pre-conception
- Methimazole
- Prophylthiouracil
Methimazole
- Medication for women with graves disease
- 1 daily dose
- Inhibits thyroperoxidase (necessary for iodination of T4 to T3)
- Maternal side effects: transient leukopenia
- Fetal side effects: “methimazole embryopathy”: aplasia cutis, esophageal atresia
- Avoid during 1st trimester
Prophylthiouracil
- Medication for women with graves disease
- 3x daily dose
- Inhibits thyroperoxidase (necessary for iodination of T4 to T3)
- Maternal side effects: liver toxicity (<1%), transient leukopenia (10%)
- Fetal side effects: none
Asthma during pregnancy
- Affects 4-8% of pregnancies
- Rule of 1/3: 1/3 get better, 1/3 stay the same, 1/3 get worse
- 24-28wks peak timing
Lung physiology During Pregnancy
In a state of chronic hyperventilation during pregnancy
- FEV1: unchanged
- PEFR: unchanged
- Minute ventilation: increase 30-50%
- Tidal volume: increased 30-50%
- FVC: unchanged
- Functional residual volume: 18-20%
- Increased minute ventilation = hyperventilation—>chronic respiratory alkalosis
- Normal CO2 in pregnant pt = impending respiratory failure
Asthma therapy during pregnancy
- 1st line: Albuterol rescue
- 2nd line: Budesonide, Fluticasone (inhaled corticosteroids)
- 3rd line: Salmeterol, Formoterol
- 4th line: Oral corticosteroids
Fetal effects of asthma medications
- Short-acting B agonists
*fetal effects: tachycardia
*maternal effects: tachycardia
- Inhaled corticosteroids
*safe for both
- Long-acting B agonists
*fetal effects: tachycardia
*maternal effects: tachycardia
- Oral corticosteroids
*fetal effects: 1st trimester: cleft lip and palate (2-3%), 3rd trimester: fetal growth restriction, premature rupture of membranes
*maternal effects: gestational diabetes
Well-controlled asthma
- No daytime or nocturnal symptoms
- No limitations on activity
- Minimal need for rescue medication
- Normal lung function
Physiology of venous thromboembolism during pregnancy
- 4x more common in pregnant women
- 20% of maternal deaths
- 50% occur postpartum
- Pregnancy is a hypercoagulable state
*increased factor VIII, IX, X, fibrinogen
*decreased fibrinolysis, antithrombin, protein S
- Other issues
*venous stasis, IVC compression
*decreased physical activity
*cesarean deliveries
Risk factors for venous thromboembolism
- Prior VTE
- Thrombophilia
- >35
- Obesity
- Parity >4
- Autoimmune, renal disease
- Personal, family history
- New onset
*varicose veins
*immobility, bedrest
*preeclampsia
*cesarean delivery
*multiple gestation
Testing for VTE
- D-dimer is of no use during pregnancy as it is elevated in all expectant mothers
- Helical CT scan (gold standard)
- V/Q scan
- Lower extremity Dopplers (DVT)
VTE Treatment
- LMWH treatment of choice
- Does not cross placenta
Warfarin embryopathy
- Exposure to warfarin at 6-11wks
- Nasal hypoplasia
- Stipled epiphyses
- CNS, optho abnormalities
- Hemorrhagic complications at delivery
- May be necessary esp w/ mechanical prosthetic valves
Antiphospholipid Antibody Syndrome
- Acquired, autoimmune disease
- Venous thrombosis (2%)
- Arterial thrombosis (20-24%)
- Pregnancy morbidity
*unexplained fetal death >10wks
*severe preeclampsia
*3+ unexplained consecutive miscarriges <10wks
- Lab criteria: lupus anticoagulant, anticardiolipin antibodies, anti-b2 glycoprotein antibodies
APLS managment
- Low-dose aspirin, prophylactic LMWH
Testing mother for inherited thrombophelia
- Should get labs and know of any family diseases
- Should not test for protein C or S during pregnancy b/c they are always going to be low
*testing for deficiency by testing protein lvls
- APLS is acquired and not inherited
*antiphospholipid antibody- acquired thrombophilia, not inherited
- Test for Facto V Leiden mutation, prothrombin gene mutation and antithrombin 3 deficiency
*prothrombin gene mutation- genetic testing, not altered
Levothyroxine
- Manufactured form of the thyroid hormone, thyroxine (T4)
- It is used to treat thyroid hormone deficiency
Neonatal Grave Disease
- IUGR
- Cachetic
- Exophthalmos
- Failure to thrive
- Due to TSIs (1% exposed)
*regardless of how mothers grave disease is treated she will still have thyroid antibodies in her blood that can cross the placenta and cause grave disease in fetus
