Maternal Physiology Flashcards
Maternal CV adaptation to pregnancy (and peak trimester)
Increased CO (increased HR, SV) - peak 2nd tri
Increased Blood volume (red cell, plasma)
Decreased SVR (response to ADH, Angio II, NE)
BP = nadir 2nd trimester
Maternal RESP adaptation to pregnancy
Increased Tidal Vol (increased chest wall exp, diaphragm excursion, mild dyspnea)
Increased MV (resp alkalosis, mild dyspnea) -> pH 7.4-7.45
Increased O2 consumption
Increased mucosal tissue activity (congested)
Maternal RENAL adaptation
Increased
- renal blood flow
- kidney size
- GFR
- collecting system dilates
- excrete more protein
- sx -> urinary frequency, urgency, incontinence
Decreased
- Cr (first up then down)
- Glucose and a.a. absorption
- Decrease Na, HCO3 (compensatory for resp alkalosis), albumin, plasma osmolality
Maternal METABOLISM adaptation
Increased
- cholesterol, triglycerides
- insulin production (estrogen -> increase pancreatic beta cells -> later.. leads to insulin resistance)
- Fe and folate requirements (for increased pRBCs)
Decrease
- fasting glucose,
- glucose tolerance
-Hba1c (b/c increase pRBCs) - falsely reassuring measures in pregnancy
Maternal LABS - different in pregnancy
wbc
D-dimer
Hepatic factors (coags, proteins in clotting cascade)
wbc ↑
hepatic factors ↑ (except PROTEIN S - “slides” but C “climbs”)
Describe placenta implantation (name cells on fetal and maternal side) - what are maternal side cells. what are fetal side cells (placenta)
Implanted by day 5
Syncitiotrophoblast - mom side
Cytotrophoblast - fetal side (placenta?)
Describe initiation of placental blood supply
Getting blood supply:
1. Columns of trophoblast develop (villi)
2. Interstitial EVT at distal edge of columns invades decidua
3. Endovascular EVT at distal edge invades endothelium and tunica
media of maternal spiral arteries
4. Spiral arteries are remodeled to become low resistance vessels
=lots of blood flow around the villi
Describe placenta blood supply from mother
Name hormones (peptide hormones) produced by placenta and their role
- human chorionic gonadotropin (HCG) - makes progesterone (keeps CL working until placenta takes over making hormones)
- human chorionic somatomammotropin / human placental lactogen - increases fetal glucose supply (anti-insulin), increases lipid utilization, starts around wk 8 and increases throughout pregnancy
- growth hormone, IGF - fetal growth
- angiogenic factors (VEGF, PLGF)
Name hormones (steroid hormones) produced by placenta and their role
- estrogen - uterus and breast devp, angiogenesis, protein synthesis, cont increase throughout pregnancy
- progesterone - smooth mm relaxation, immunosuppressant, GI sx - start to decrease (or less function) around time of delivery so less relaxation of uterus
- glucocorticoid
Describe molar pregnancy (when it occurs)
abnormal imprinting - excess of PATERNAL chromosome material (imprinting affects PLACENTAL development) - partial mole if some oocyte, complete mole if no oocyte
abnormal villi, trophoblast proliferation, villous edema
Describe mole - no fetus, no amnion, 46 XX, LARGER placenta
LT risks
BCG elevates RAPIDLY
Complete molar pregnancy
20% risk trophoblastic tumors
Describe molar pregnancy –
nonviable fetus, 69 XXY or 69 XXX, small uterus
Partial molar pregnancy
Describe gestational trophoblastic disease
imprinted genes gone completely awry
invasive mole
eg choriocarcinoma - invade uterine blood vessels
How does gas exchange occur in placenta?
What can impact this gas exchange?
Simple diffusion of CO2 and O2
Ischemic placental disorders eg PEC, IUGR
Abnormally large placenta eg molar, hydrops, mult gestation
How do various nutrients cross into placenta?
- Simple diffusion
- Facilitated diffusion
- Active transport
- Pinocytosis
Glucose - facilitated diffusion, supported by GLUT 1
Amino acids - active transport, carrier protein
FFA - esp arachidonic acid, docosahexaminoic acid (?) - imp for brain devp , myelination
Describe marginal cord insertion.
Describe velamentous cord insertion.
Marginal - cord inserts at margins rather than center of the placenta. Could affect fetal growth.
Velamentous - umbilical vessels diverge as they traverse between the amnion and chorion before reaching the placenta so exposed vessels (not in wharton jelly) and longer route - can affect fetal nutrition, also risk of bleeding.
Describe placenta previa
Describe vasa previa
Describe placenta accreta spectrum
Risks associated with each
Delivery indications
- Highest risk with placenta previa and prior cesarean deliveries
previa - over/near cervix
vasa previa - umb vessels over/near cervix
PAS - abnormal trophoblast invasion into the myometrium, sometimes beyond serosa.
usually late preterm delivery, for PAS - +hysterectomy
Gestational diabetes vs Pre-gestational diabetes
definition, perinatal risks, fetal complications
GDM - macrosomia, operative delivery, septal hypertrophy (resolves in few months); rx can decrease perinatal complications; 80% women devp dmII, metabolic syndrome
Dx: screen 24 - 28 wks
Dx: > 130 - 140 ; 1 hr -> 3 hr test; 2 abnormal = + dx
Dx: > 200
Pre-gestational DM
- Type 1 risk DKA,
- Type 2 ins resistance of pancreatic beta cells - more like GDM risks
Risk congenital malformations (early in pregnancy 5 - 8weeks)
- cardiac (#1 cardiac TGA, conotruncal eg truncus, VSD, septal), CNS (holoprocencephaly, caudal regression), GI (small L colon), renal, GU, skeletal (#1 malf - caudal regression), small vessel injury (FGR)
Best way to decrease perinatal complications of pre-gestational diabetes
Good pre-gestational glycemic control
Newborn IDM presentation can include…
Hypocalcemia
Hypoglycemia
Polycythemia (from increased EPO - uterine hypoxia?)
Define gestational hypertension - when can you make definitive diagnosis?
Define pre-eclampsia
Define sPEC
Define HELLP
Eclampsia (rx)
Primary RFs
gHTN - >= 140 or >= 90 in previously normotensive, defn dx post-pregnancy
PEC -> as above + proteinuria AFTER 20 wks or w/o proteinuria but sx (visual, renal, LFTs, pulmonary edema)
HELLP - Hemolysis (LDH>600, BR> 1.2, PBS), Elevated Liver enzymes, Low Platelets (<100) (may or may not have proteinuria or even HTN)
Eclampsia - seizure w/o other etiology - > Mg, delivery!
RF - primigravida, cHTN, twins, DM, obesity
Dx severe PEC
HTN + proteinuria + 1 of these:
- BP > 160/110 (2X, 6 hrs apart)
- proteinuria > 5g/24 hrs or 3+ x 2
- change vision, headache, oliguria, any HELLP, pulm edema, FGR
Fetal impact of mat hypertension
Thrombocytopenia
* Neutropenia
* Polycythemia
* Hypocalcemia from maternal
magnesium sulfate
* Reduced nephron number
* Later in adulthood-diabetes, high
blood pressure, heart disease
Maternal thyroid disease
- most common cause of neonatal hyperthyroidism (describe it)
mat graves (placental transfer of stimulating TSH-R antibodies)
What does fetal thyroid devp contribute to? depend on?
maturation of thyroid dep tissues including brain, linear growth
depends on maternal I intake, TSH does NOT cross placenta
Complications of neonatal graves
Fetal complications
Neonatal complications
- when do sx occur?
Neonatal thyrotoxicosis
Fetal
* Fetal tachycardia
* Growth restriction
* Fetal hydrops
* Fetal goiter
Neonatal
* Irritability
* Excessive movement
* Tremor
* Flushing of the cheeks
* Sweating
* Increased appetite
* Weight loss or lack of weight gain
* Supraventricular tachycardia
* Goiter
* Exophthalmos
24 hours
TSH-R ab levels 500% above normal
Thyrotoxicosis
* Hyperthermia
* Arrhythmia
* High-output cardiac failure may occur
* Death
Note - a small % of infants may be hypothyroid (more TSH-R inhibiting antibodies cross than TSH-R stimulating antibodies); rest would be hyperthyroid
NOTE: antibodies deplete in about 3 - 12 weeks
Neonatal hypothyrodism
- Most “common” causes
- Clinical manifestations
congenital goiter
transient neonatal hypothyroidism (TSH-R BLOCKING ab transfer, maternal I deficiency, exposure to mat anti-thyroid meds or post-natal exposure to excess Iodine eg betadine), mat meds eg amiodarone
- PTB/LBW
- Placental abruption
- Preeclampsia and assoc fetal/neonatal features
*Neonatal neurocognitive impairment!
Maternal lupus
Complications to fetus
- cardiac (timing of presentation)
- skin
Heart block - 2% born to mothers with +anti-SSa or +anti-SSB (1st, 2nd or 3rd).
- Present 18 - 25 weeks. Could have hydrops.
- 80 - 95% of congenital heart block due to SLE (antibodies, indep of disease state).
- NOT reversible
Skin - 4 to 16% of +antibody. Can present at birth; usually w/in a few weeks. Annular, macular, centrally light esp scalp, peri-orbital region.
Drugs contraindicated in pregnancy (and complications)
Drugs inhibiting RAAS eg ACE, ARB
- impaired fetal/neonatal renal function -> oligohydramnios during pregnancy (with pulmonary hypoplasia)
- anuria and renal failure after delivery
- ESP in 2nd and 3rd trimester = bad
Neonatal Abstinence Syndrome
Neonatal Opiate Withdrawal Syndrome
- are sx mat dose dependent?
- presentation of sx
- seizures?
Not, not dose dep although may be in methadone
Sx of NAS
10% with sz, 30% with EEG changes not ax with sz
Timing of onset of NAS sx
- opioids
- methadone
- buprenorphine
- Heroin-within 24 hours
- Methadone-24-72 hours
- Buprenorphine-onset peaks at 40 hours, most severe at 70 hours
Fetal Alcohol Syndrome
- how does alcohol cross placenta
- fetal complications
- neonatal complications
Alcohol is the most damaging substance to the fetus used
during pregnancy.
Freely crosses placenta.
Damage in fetal brain due to:
* Exposure to alcohol leads to apoptosis during development
* Formation of free oxygen radicals, which damage cell membranes via lipid peroxidation, leading to cell death
Neonatal
- IUGR
- facial features - smooth philtrum, thin upper lip, small eye opening
- neurocognitive
- other organs
FAS is the leading cause of intellectual disability in Western Hemisphere
