Maternal Disease in Pregnancy; Diseases of Pregnancy Flashcards
4 Types of HTN in pregnancy
- chronic HTN
- gestational
- pre-eclampsia
- pre-eclampsia superimposed on chronic HTN
Definition of chronic HTN in pregnancy
- defined as sustained BP >140/90 on 2 occasions btw 6hr and 7d apart
- defined as diagnosis of chronic HTN prior to pregnancy, prior to week 20 of gestation, or persisting beyond day 42 post-partum
Management of chronic HTN in pregnancy
- DO: establish pre-preg baseline data, monitor kidney function and labs (proteinuria, Cre, LFTs, LDH, uric acid), get EKG/Echo, and ophthalmic exam if long-standing HTN; start meds if SBP>150/160 or DBP>100-110; dietary change and quit smoking; serial growth US starting at 32wks, deliver by 39wk if no other complications (otherwise deliver earlier)
- management DON’Ts: don’t give ACEIs or ARBs, best not to give diuretics, don’t encourage weight loss
- *Consider hyperaldosteronism and molar pregnancy if severe range BPs prior to 20wk; work up for SLE/RD if proteinuria is disproportionate to HTN
What are the safe options for anti-HTN medications in pregnancy?
- Methyldopa (central alpha agonist, AEs: hepatitis, hemolytic anemia)
- Labetalol (beta blocker with some anti-alpha activity, AEs: flushing, HA, tremulousness)
- Nifedipine (Ca channel blocker, AEs: HA, tachycardia, ortho-hypo)
- Thiazide diuretics
- Hydralazine
Describe insulin resistance and pregnancy
- pregnancy hormones contribute to insulin resistance
- insulin resistance is highest in the 3rd trimester
- can lead to gestational DM2, which involves significant M&M (SAB, malformations, hyperglycemia, macrosomia, shoulder dystocia, death, neonatal complications, retinopathy, nephropathy, DKA, exacerbation of gastroparesis)
Appropriate pre-conception management for a patient with DM2 includes…
- HgbA1c
Appropriate antepartum management for a pt with DM2 includes…
- baseline evaluation (labs - urine protein, cre, Hgb A1c, TFTs, urinalysis, urine culture; fundoscopic eval, BP and EKG)
- pursue goals of gluc control, Hgb A1c
What is the preferred insulin regimen in pregnancy and delivery?
Antepartum:
- best regimen includes bid injections of NPH and Novolog
- dosing = 2:1 ratio in AM; 1:1 ratio in PM
- will need to increase insulin each trimester
Intrapartum:
- int. acting insulin at bedtime; hold morning dose
- latent labor: give IV saline; monitor BG q2-4hr
- active labor: give 5% dextrose; check BG q1hr and maintain at 100, if above 110 give short acting insulin
Testing for gestational DM
- low-risk: 1hr 50gm GCT btw 24-28wks
- high-risk: 3hr 100gm OGTT at start of prenatal care
- high-risk = women with hx of GDM, macrosomia, stillbirth or congenital anomaly, PCOS, 1˚ relative with DM2, or pre-diabetes
- can avoid screening in women
Antepartum and intrapartum management of Gestational DM
Same as with DM2:
- insulin preferred, Glyburide/Metformin also options; monitor baby more closely as it gets closer to term
- latent and active labor are same recs too
- post-partum: 15-50% will develop DM2 later, up to 1/3 will still have impaired glu metabolism at post-partum screening
Neonate of the diabetic mother
- may have hypoglycemia, correlated with degree of maternal gluc control 6wk prior to delivery
- elevated insulin + chronic pancreatic hypertrophy –> umbilical nutrient disruption –> sig hypoglycemia in the baby
- uncorrected neonatal hypoglycemia can lead to seizures, brain damage, death
- manage with BG checks, early oral feedings, IV gluc if feeding is insufficient
Breastfeeding in Diabetic mother
- concern is that it will make her hypoglycemic, but a small snack just before will reduce that
- will reduce/delay the risk of subsequent DM in the kid
Normal thyroid changes in pregnancy
- normally thyroid gets a little bigger in pregnancy and the mother has inc. TBG, inc. renal excretion of iodide
- 1st trimester: estrogen inc. TBG production and extends half-life, get 2.5-fold inc. in TBG; hCG structural similar to TSH so binds TSHR, stimulates thyroid; net effect is increased pool of TH, unchanged free TH, suppressed TSH
- 2nd trimester: dec. hCG, TSH normalized
- placenta allows pretty much all TH stuff through but not TSH
Thyroid disease in pregnancy
- hyperthyroidism (0.2%) - 95% of cases are Graves; tx with PTU in 1st trim, Methimazole in 2nd/3rd trim, +/- beta-blockers; if untx’d may get IUGR, pre-term birth, preeclampsia
- hypothyroidism (2.5%) - 95% of cases are Hashimoto’s; tx with Levothyroxine, inc. q4wk, mean inc. ~45%; if intx’d may get preeclampsia, anemia, low birth wt (2/2 preterm delivery 2/2 PIH), abruption, fetal death, under-neuro-developed
- screen for thyroid dysfunction if there’s hx of thyroid dz, AI dz, DM1, fam hx, symptomatic, or goiter
- best way to screen is check TSH - if normal, no further work-up; low indicates hyperthyroid, high indicates hypothyroid; routine screening not recommended
Describe some risk factors for premature rupture of membranes (PROM).
** intrauterine infection ** Prior hx of PROM or preterm labor Cervical insuff. Polyhydramnios Mult. gest. Trauma Fetal malformations Amniocentesis Low soc. ec. status Smoking STIs
Describe some M&M of premature rupture of membranes (PROM).
Chorioamnionitis Preterm L&D Placental abruption Umb. cord prolapse Seq. of prematurity Pulm. hypoplasia Potters-like sequence Thromboembolic dz due to bedrest (mom)
Do you stick your fingers in a woman that has a suspected mass of fluid waiting to blow out of her cervix if angered?
What else can you do to examine a pt suspected of having preterm membrane rupture?
Nope. Don't do that. Take vitals, incl. temp. Assess for fundal tenderness Sterile speculum exam Ultrasound FHR and contraction monitoring
Describe the management of PROM @ 34 wks or greater and at
> 34 wks: proceed w/ delivery.
Define preterm delivery (PTD).
Contractions that cause cervical change before 37 wks gestation.
Describe the RFs for preterm delivery.
Prior hx of PTD.
Ifxn
Uterine malformations
Uterine distension
Vag. bleeding (2ndary to placenta previa/abruption)
Cervical insuff.
Smoking, cocaine, non-white race, low sec. econ. status…
Describe the short and long-term neonatal consequences of PTD.
Short term: RDS, hypothermia, jaundice, hypoglycemia, intraventricular hemorrhage, necrotizing enterocolitis, bronchopulmonary dysplasia, sepsis, PDA.
Long term: cerebral palsy, mental retardation, retinopathy of prematurity
