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Neo boards > Maternal Physiology > Flashcards

Maternal Physiology Flashcards

1
Q

Maternal CV adaptation to pregnancy (and peak trimester)

A

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

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2
Q

Maternal RESP adaptation to pregnancy

A

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)

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3
Q

Maternal RENAL adaptation

A

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

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4
Q

Maternal METABOLISM adaptation

A

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

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5
Q

Maternal LABS - different in pregnancy

wbc
D-dimer
Hepatic factors (coags, proteins in clotting cascade)

A

wbc ↑
hepatic factors ↑ (except PROTEIN S - “slides” but C “climbs”)

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6
Q

Describe placenta implantation (name cells on fetal and maternal side) - what are maternal side cells. what are fetal side cells (placenta)

A

Implanted by day 5

Syncitiotrophoblast - mom side
Cytotrophoblast - fetal side (placenta?)

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7
Q

Describe initiation of placental blood supply

A

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

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8
Q

Describe placenta blood supply from mother

A
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9
Q

Name hormones (peptide hormones) produced by placenta and their role

A
  • 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)
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10
Q

Name hormones (steroid hormones) produced by placenta and their role

A
  • 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
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11
Q

Describe molar pregnancy (when it occurs)

A

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

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12
Q

Describe mole - no fetus, no amnion, 46 XX, LARGER placenta

LT risks

BCG elevates RAPIDLY

A

Complete molar pregnancy

20% risk trophoblastic tumors

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13
Q

Describe molar pregnancy –

nonviable fetus, 69 XXY or 69 XXX, small uterus

A

Partial molar pregnancy

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14
Q

Describe gestational trophoblastic disease

A

imprinted genes gone completely awry

invasive mole

eg choriocarcinoma - invade uterine blood vessels

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15
Q

How does gas exchange occur in placenta?

What can impact this gas exchange?

A

Simple diffusion of CO2 and O2

Ischemic placental disorders eg PEC, IUGR

Abnormally large placenta eg molar, hydrops, mult gestation

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16
Q

How do various nutrients cross into placenta?

  • Simple diffusion
  • Facilitated diffusion
  • Active transport
  • Pinocytosis
A

Glucose - facilitated diffusion, supported by GLUT 1

Amino acids - active transport, carrier protein

FFA - esp arachidonic acid, docosahexaminoic acid (?) - imp for brain devp , myelination

17
Q

Describe marginal cord insertion.
Describe velamentous cord insertion.

A

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.

18
Q

Describe placenta previa
Describe vasa previa
Describe placenta accreta spectrum

Risks associated with each

Delivery indications

A
  • 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

19
Q

Gestational diabetes vs Pre-gestational diabetes

definition, perinatal risks, fetal complications

A

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)

20
Q

Best way to decrease perinatal complications of pre-gestational diabetes

A

Good pre-gestational glycemic control

21
Q

Newborn IDM presentation can include…

A

Hypocalcemia
Hypoglycemia
Polycythemia (from increased EPO - uterine hypoxia?)

22
Q

Define gestational hypertension - when can you make definitive diagnosis?

Define pre-eclampsia

Define sPEC

Define HELLP

Eclampsia (rx)

Primary RFs

A

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

23
Q

Dx severe PEC

A

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
24
Q

Fetal impact of mat hypertension

A

Thrombocytopenia
* Neutropenia
* Polycythemia
* Hypocalcemia from maternal
magnesium sulfate
* Reduced nephron number
* Later in adulthood-diabetes, high
blood pressure, heart disease

25
Q

Maternal thyroid disease

  • most common cause of neonatal hyperthyroidism (describe it)
A

mat graves (placental transfer of stimulating TSH-R antibodies)

26
Q

What does fetal thyroid devp contribute to? depend on?

A

maturation of thyroid dep tissues including brain, linear growth

depends on maternal I intake, TSH does NOT cross placenta

27
Q

Complications of neonatal graves

Fetal complications

Neonatal complications

  • when do sx occur?

Neonatal thyrotoxicosis

A

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

28
Q

Neonatal hypothyrodism

  • Most “common” causes
  • Clinical manifestations
A

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!
29
Q

Maternal lupus

Complications to fetus
- cardiac (timing of presentation)
- skin

A

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.

30
Q

Drugs contraindicated in pregnancy (and complications)

A

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

31
Q

Neonatal Abstinence Syndrome

Neonatal Opiate Withdrawal Syndrome

  • are sx mat dose dependent?
  • presentation of sx
  • seizures?
A

Not, not dose dep although may be in methadone

Sx of NAS

10% with sz, 30% with EEG changes not ax with sz

32
Q

Timing of onset of NAS sx
- opioids
- methadone
- buprenorphine

A
  • Heroin-within 24 hours
  • Methadone-24-72 hours
  • Buprenorphine-onset peaks at 40 hours, most severe at 70 hours
33
Q

Fetal Alcohol Syndrome

  • how does alcohol cross placenta
  • fetal complications
  • neonatal complications
A

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

Neo boards (14 decks)

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