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RGU Exam 2 > Medical Complications of Pregnancy > Flashcards

Medical Complications of Pregnancy Flashcards

1
Q

Changes in insulin requirements for Type 1 diabetics during pregnancy

A

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
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2
Q

Glucose toxicity to fetus

A
  • 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
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3
Q

Important time periods during pregnancy

A
  • <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

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4
Q

HbA1c value vs risk of major malformation

A
  • 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
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5
Q

Fetal complications of diabetics mothers

A
  • Macrosomia (birth weight >9lbs)

*carries a high risk of birth injury; shoulder dystocia, brachial plexus injury

  • Miscarriage
  • Neonatal complications

*respiratory distress

*jaundice

*hypoglycemia

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6
Q

Maternal complications with diabetes

A
  • 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
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7
Q

ACE inhibitors during pregnancy

A
  • Cause birth defects
  • Increased heart defect
  • Can cause permanent renal dmg, oligohydramnios
  • Fetuses w/ renal dysplasia are typically not compatible w/ life
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8
Q

Medication regimen for diabetics during pregnancy

A
  • Switch from oral meds to insulin
  • Stop ACEI, ARBs
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9
Q

Maternal thyroid physiology during pregnancy

A
  • 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)

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10
Q

Thyroid hormones to monitor during pregnancy

A
  • Want to check the free ones
  • Free T3 and T4 are the only ones you want to watch during pregnancy
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11
Q

Fetal thryoid development

A
  • 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
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12
Q

hCG effect on thyroid

A
  • Can have a transient effect in increasing thyroid function by mimicing TSH resulting in lower levels of TSH
  • Can mimic a hyperthyroidism
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13
Q

Iodine deficiency in fetus

A
  • 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
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14
Q

Thyroid function across placenta

A
  • 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
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15
Q

Fetal complications of hyperthyroidism

A
  • Growth restriction
  • Prematurity
  • Stillbirth
  • Miscarriage
  • Tachycardia
  • Goiter
  • Preeclampsia
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16
Q

Maternal Graves Disease Medication options

A
  • Women w/ grave should be treated medically or undergo ablation pre-conception
  • Methimazole
  • Prophylthiouracil
17
Q

Methimazole

A
  • 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
18
Q

Prophylthiouracil

A
  • 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
19
Q

Asthma during pregnancy

A
  • 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
20
Q

Lung physiology During Pregnancy

A

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
21
Q

Asthma therapy during pregnancy

A
  • 1st line: Albuterol rescue
  • 2nd line: Budesonide, Fluticasone (inhaled corticosteroids)
  • 3rd line: Salmeterol, Formoterol
  • 4th line: Oral corticosteroids
22
Q

Fetal effects of asthma medications

A
  • 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

23
Q

Well-controlled asthma

A
  • No daytime or nocturnal symptoms
  • No limitations on activity
  • Minimal need for rescue medication
  • Normal lung function
24
Q

Physiology of venous thromboembolism during pregnancy

A
  • 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

25
Q

Risk factors for venous thromboembolism

A
  • Prior VTE
  • Thrombophilia
  • >35
  • Obesity
  • Parity >4
  • Autoimmune, renal disease
  • Personal, family history
  • New onset

*varicose veins

*immobility, bedrest

*preeclampsia

*cesarean delivery

*multiple gestation

26
Q

Testing for VTE

A
  • 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)
27
Q

VTE Treatment

A
  • LMWH treatment of choice
  • Does not cross placenta
28
Q

Warfarin embryopathy

A
  • 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
29
Q

Antiphospholipid Antibody Syndrome

A
  • 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
30
Q

APLS managment

A
  • Low-dose aspirin, prophylactic LMWH
31
Q

Testing mother for inherited thrombophelia

A
  • 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

32
Q

Levothyroxine

A
  • Manufactured form of the thyroid hormone, thyroxine (T4)
  • It is used to treat thyroid hormone deficiency
33
Q

Neonatal Grave Disease

A
  • 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

RGU Exam 2 (21 decks)

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