Maternal/Fetus/Transition Flashcards
Type of twins most at-risk for twin-twin transfusion syndrome (TTTS)
Monochorionic–most commonly mono-di, rarely in mono-mono
By sharing chorion can have multiple placental anastamoses so blood flow can become imbalanced
Signs (by escalating level of severity) of twin-twin transfusion syndrome (TTTS)
I: poly/oligo-hydramnios
II: absent bladder (donor)–this and anything more warrants laser occlusion/ablation
III: abnormal doppler flows (signifying insufficient delivery to donor)
IV: hydrops (recipient)
V: demise
(Quintero staging)
Risks to donor in twin-twin transfusion syndrome (TTTS)
Growth restriction
Anemia
“Stuck” (adhering to membranes 2-2 severe olighydramnios)
Death (higher risk to donor>recipient)
Risks to recipient in twin-twin transfusion syndrome (TTTS)
Hypervolemia/hydrops
Polycythemia
High-output heart failure/hypertrophic cardiomyopathy
Disseminated intravascular coagulopathy and thromboembolic events
Demise (higher risk in donor)
If one twin dies in-utero from twin-twin transfusion syndrome, the other has ____% risk of demise
>30%
(Often within hours; sudden shift in blood flow from pressure-drop in dead twin’s system steals from survivor–severe hypoperfusion)
Definition of preeclampsia and severe preeclampsia
- SBP>140 or DBP>90 plus proteinuria
- SBP>160 or DBP>110 plus proteinuria
Quad screen findings for Trisomy 21
Low AFP, high bHCG, low estradiol, high inhibin
Put in alphabetical order and then alternates low-high-low-high (remember it “starts” with low because only open defects cause high AFP)
What do late decelerations indicate?
Fetal hypoxemia
Most classic term is “uteroplacental insufficiency”
Teratogenic effects of Isotretinoin
dTGA
Macrocephaly, triangular faces
_T_retinoin = _T_GA and _T_riangular _T_oo big head
What is the most identifiable common cause of non-immune hydrops
Cardiac abnormalities (arryhthmias [which are often associated with CHD])
Account for 25% of non-immune hydrops
What three organs are prioritized for oxygen delivery/blood flow
Adrenals
Brain
Coronaries (heart)
Umbilical vein blood has a pO2 of ____
30mmHg (half the lower-limit of normal ex-utero)
About 1/3 of this oxygenated blood bypasses to the aorta through the foramen ovale (since it’s ejected pre-DA, it goes to most oxygen-needy coronaries and head)
A THIRD of this THIRTY mmHg blood goes to the THIRSTY heart and brain
How IgG transplacentally transferred
Pinocytosis
Really only molecule tested that’s transferred this way
The treatments mothers with a prior infant with Neonatal Alloimmune Thrombocytopenia (NAIT) receive
Steroids and weekly IVIG
Start at 12 weeks if prior infant had intracranial hemorrhage (ICH) (20 weeks if no prior ICH)
Most common cause of mild thrombocytopenia in a well-appearing newborn
Placental insufficiency
(Most common cause of severe thrombocytopenia is NAIT)
What do the umbilical arteries branch off of
Umbilical arteries come off the internal iliac arteries
Which ventricle provides majority of fetal cardiac output
Right (66% of CO)
Why it’s relatively hypertrophied at birth
What are the PO2/oxygen saturations in the:
1) Umbilical vein
2) Left ventricle
3) Right ventricle
4) IVC/SVC
1) UV: PO2 40 / SaO2 80% (DV SaO2 70% per Brodsky)
2) LV: PO2 30 / SaO2 65%
3) RV: SaO2 55%
4) SVC/IVC: PO2 15 / SaO2 30%
* (Some variation in quoted numbers in literature, these picked as representative and easy to remember)*
The right-heart pressure is _____ the left-heart because of ________
- EQUAL TO
- Large shunts (foramen ovale and ductus arteriosus)
In-utero, prostaglandins come from ______ and ex-utero, they’re metabolized _________
The placenta
In the lung vasculature
Increased PBF→faster metabolism→closure of PDA→more PBF (PBF=pulmonary blood flow)
What two arteries constrict with increasing PaO2
Umbilical arteries
Ductus arteriosus
Most heart defects occur by ___ weeks of gestation
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