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Neo boards > MFM > Flashcards

MFM Flashcards

1
Q

Define TTTS

Define TAPS

A

●TTTS – TTTS is characterized by relative hypovolemia of one twin (donor) and hypervolemia of the other twin (recipient) as a result of imbalance in the direction of flow through the placental anastomoses.

●TAPS – TAPS is an atypical chronic form of TTTS caused by slow transfusion of red blood cells through a few very small (<1 mm diameter) placental anastomoses with net increased unidirectional flow, resulting in anemia of one twin and polycythemia of the co-twin Amniotic fluid volumes are normal. The cardinal prenatal finding is MC placentation with middle cerebral artery-peak systolic velocity greater than 1.5 multiples of median (MoM) in one twin and less than 0.8 MoM in the other twin. TAPS may occur spontaneously or after laser therapy of TTTS.

Hypoperfusion of the kidneys of the chronically hypovolemic twin (called the donor twin) results in activation of the renin-angiotensin-aldosterone system (RAAS) and release of angiotensin II, renin, aldosterone, and vasopressin in an ongoing attempt to restore its intravascular volume and maintain its blood pressure [6,7]. This leads to oliguria, with anhydramnios.

Chronic hypervolemia in the recipient twin causes its cardiac atria to stretch and release atrial natriuretic peptide; ventricular stretch results in release of brain natriuretic peptide [8]. These hormones promote vasodilation, natriuresis, and inhibition of the RAAS, leading to polyuria and polyhydramnios. Over time, however, the recipient can develop hypertensive cardiomyopathy as a result of ongoing volume overload, elevated levels of endothelin I, and elevated levels of RAAS mediators that it acquires from the donor through the AV anastomoses, even though its own RAAS system is down-regulated [9-11]. Venous hypertension is a late stage of the process and results in movement of intravascular fluid into the interstitial spaces and functional lymphatic obstruction, leading to hydrops fetalis

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2
Q

Teratogenic effect - name that drug

  • Decreased fetal growth
  • Worse neurodevelopmental outcomes
  • Still much studies need to be conducted esp transfer in BM
A

Marijuana

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3
Q

Teratogenic effect - name that drug

  • Oligohydramnios
  • Hypoplasia of skull
  • Fetal compression syndrome (limb deformities) +/- pulm hypoplasia
  • Renal tubular dysgenesis
A

ACE inhibitors

GREATER risk of during 2nd and 3rd trimester

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4
Q

Teratogenic effect - name that drug

Facial - high forehead, broad nasal bridge, anteverted nostrils, midface hypoplasia, long philtrum

Cardiac - range CHD including CoA, HLH, AV stenosis, etc

Extremities - LONG thin fingers and toes, HYPERCONVEX fingernails

Neurology - NTD (eg MMC esp 1st trimester exposure), ID maybe

A

Valproic acid

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5
Q

Teratogenic effect - name that drug

Cleft lip
Cleft palate
Cardiac abnormalities
Increased risk of WITHDRAWAL
Increased risk hemorrhaghic disease of NB (decreased vit K placental transfer)

A

Phenobarbital

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6
Q

Teratogenic effect - name that drug

Vaginal adenocarcinoma
Abn female reproductive organ devp
Abn male reproductive organ devp

A

DES- diethylstilbestrol

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7
Q

Teratogenic effect - name that drug

Spont abortion and STILLBIRTH

Cardiac - TGA, truncus, ToF, etc

Facial - MICROTIA or ANOTIA +/-stenosis of external ear canal, may have down slanting palpebral fissures, hypoplastic maxilla and mandible (triangular facies), U shaped cleft palate, narrow sloped forehead

Neurology - hydrocephalus, cerebellar hypoplasia, microcephaly, ID

Other - limb reduction, thymic or PTH abn

A

Isotretinoin / Retinoic acid

abnormalities only described w. 1st trimester exposure

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8
Q

Teratogenic effect - name that drug

Facial - NASAL HYPOPLASIA, depressed nasal bridge, deep groove between nasal alae and tip

Neuro - severe ID, sz, microcephaly

Ortho - STIPPLED bone epipheses

Other - mild nail hypoplasia

Worst if exposure 6 - 12 weeks GA then decrease effects if exposure > 12 weeks GA

A

Warfarin

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9
Q

Teratogenic effect - name that drug

Most common teratogenic exposure to fetus

Must have abnormalities in 3 areas:

  • Physical
    — Facial - long, smooth philtrum, thin upper lip. short palpebral fissures, strabismus, short nose
    — Cardiac - VSD > ASD, ToF
  • Growth - IUGR, short stature
  • Neurodevelopment - irritable, tremulousness (selflimited), lower IQ, microcephaly, heterotopias, fine motor dysfunction
A

Alcohol

  • earlier exposure = greater classical features
  • worse with binge drinking vs. chronic small volume exposure
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10
Q

Teratogenic effect - name that drug

Craniofacial defects
Fingernail HYPOPLASIA
Growth restriction
Neural tube defects (MMC), ID
Decreased Vit K transfer across placenta

A

Carbamezapine

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11
Q

Teratogenic effect - name that drug

Ebstein’s anomaly

+/- goiter, seizures, DI

A

Lithium

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12
Q

Teratogenic effect - name that drug

Extremities - PHOCOMELIA, hypoplastic or absent radius, ulna or humerus, may have malformed hand

Facia - midline facial hemangioma, MICROTIA

Other - int atresia, CHD

A

Thalidomide

  • Day 27 to 33 after conception
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13
Q

Teratogenic effect - name that drug

Facial - cleft lip/palate, short nose, depressed nasal bridge

Extr - DIGIT and NAIL HYPOPLASIA

Other - growth restriction, mild ID, WIDE ANT FONTANEL, SHORT NECK, rib anomalies

Decreased Vit K transfer placenta

A

Hydantoin (Phenytoin)

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14
Q

Teratogenic effect - name that drug

Placental insufficiency - vasoconstriction in uterine circulation and uteroplacental BF / placenta with microinfarcts, atrophic villi

PTL, spont abortion, growth restriction, placenta abruption, previa

Microcephaly, maybe lung disease later in life, SIDS (?)

A

Cigarette smoking

Effects related to # of cigarettes per day (esp >10 cigarettes per day)

Nicotine increases catecholamine –> vasoconstriction uterine circulation

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15
Q

Teratogenic effect - name that drug

Increased stillbirth
Placental abruption
CUTIS APLASIA
Ileal atresia
Cardiac anomalies
Porencephaly

A

Cocaine

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16
Q

Teratogenic effect - name that drug

Facial - CRANIAL DYSPLASIA, broad nasal bridge, LOW SET EARS, wide fontanel, synostosis

Neuro - Microcephaly

A

Methotrexate

6 - 8 weeks after conception = CRITICAL period of exposure

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17
Q

Teratogenic effect - name that drug

Possible risk thrombocytopenia and bleeding

Possible intrauterine closure of PDA and pphn

A

Salicylates

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18
Q

Teratogenic effect - name that drug

Yellow brown discoloration of deciduous teeth

Can be deposited in fetal long bones

A

Tetracycline

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19
Q

How blood flows from mother to fetus; how facilitated diffusion occurs and gas exchange

A
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20
Q

Maternal compounds that DO NOT cross placenta

A

Heparin
Insulin
GLucagon
TSH
Propylthiouracil (small amounts cross)
Human growth hormone
IgM

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21
Q

What crosses placenta via simple diffusion?

A

Oxygen, CO2, H2O
Na, Cl
Lipids, fat soluble vitamins
Most meds

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22
Q

What crosses placenta via ACTIVE TRANSPORT?

A

Amino acids
Ca, Ph
Water soluble vitamins
Fe
I

(those substances that you want to be higher concentration in fetus – so needs active transport to go from lower to higher concentration / against gradient)

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23
Q

KB test and fetal blood calculation

A

KB = % fetal RBCs

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24
Q

Key factors for screening

A

1st tri PAPP-A, b-HCG 10 - 13 wks

NT 1st tri 0.5 to 2 mm

Quad 14 - 20 wks, 16 ideal
AFP least sensitive
bHCG most sensitive for tri 21
NOT helpful for tri 13
Tri 21 - down, up, down, up
Tri18 - all down

Cell free DNA > 9 wks (if too early, then low fetal DNA)

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25
Q

Types of screening approaches

A

Integrated

Stepwise

Contingent

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26
Q

Invasive screening - Amniocentesis

timing, advantages to other methods

A

15 - 20 weeks

Higher fetal loss if done earlier

Safer than CVS, less fetal injury

For - chromosomal analysis, microarray, amniotic fluid AFP, BR in Rh-sens patients, PCR for CMV, toxo

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27
Q

Invasive screening - CVS

  • timing,
  • advantages
A

10 - 13 weeks

Can be done earlier
2% are normal but have abnormal karyotype due to placental mosaicism so need to repeat 2nd trimester

Use for chr analysis of trophoblastic cells (needle into edge of placenta), dx spec gene or biochemical disorders, slightly higher fetal loss tho still < 1%,&raquo_space; if transcervical vs transabd approach

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28
Q

Invasive screening - PUBS

A

> 19 weeks
int umb vein where it inserts into placenta

For chr analysis, microarray, hct, HI hydrops

1 - 2% loss rate

rapid analysis

can give therapy eg pRBCs

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29
Q

Components of BPP

  • Go through algorithm for each BPP score and when to delivery (also based on GA > 36 wks)
A

6 + oligo -> ? delivery
6 + AFI wnl + > 36 wks -> ? delivery
6 + AFI wnl + repeat 6 mult times -> delivery

4 -> one more change repeat in 6 hrs -> no change - > deliver

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30
Q

Reactive NST

A

2 or more accels in 20 minutes with fetal movements and increase> 15bpm for > 15 seconds

predicts survival for next 7days

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31
Q

Non-reactive NST - >next step

A

rule out fetal sleep

repeat in 20 minutes, 75% are reactive

still non-reactive –> suggests fetal acidosis –> need additional evaluation

32
Q

Contraction stress test

  • what is an adequate contraction?
  • No decels -> next step
  • Intermittent late or var decels -> next step
  • Late decels > 50% of contractions -> next step
A

fetal response to contractions b/c a fetus with poor oxygenation would be even more hypoxemic with a contraction (stress)

good contraction - 3 that are 45 - 60 sec OR 1 long one (90 sec)

No decel - repeat q7days (predicts 7d survival)
Int late/var - repeat in 24 hours
+ test -> delivery if TERM, monitor FHR, BPP if PRETERM and consider steroids

33
Q

Describe category I, II and III fetal heart rate tracings

A
34
Q
A
35
Q

Decel type

A

late

36
Q

Decel type

A
37
Q

Decel type

A

sinusoidal

38
Q
A
39
Q
A
40
Q
A
41
Q

What does and does not cross placenta

A
42
Q

Review

  • site of erythropoeisis over in utero fetal development
  • changes in hemoglobin chains during fetal development and post-natal period
A
43
Q
A
44
Q

Volume of fetal blood in the maternal circulation based on KB test

A

Fetal whole blood (mL) =
(% fetal blood cells) x (maternal Hct/fetal Hct) x maternal blood volume (mL))
Fetal whole blood (mL) = (% fetal blood cells) x 5,000 mL

45
Q

Calculate amount of rhogham to give

A

Fetal blood (mL) / 30

if decimal < 0.5 then round down + 1
if decimal > 0.5 then round down + 1

eg 4.2 -> 5 vials
eg 4.7 -> 6 vials

46
Q

Review FHR tracing categories

A
47
Q
A

A

48
Q
A

C

49
Q
A

A

50
Q
A

C

51
Q
A

A

52
Q

Explains why decels occur

A
53
Q

HELLP dx

A
54
Q
A

Description of twin types and complications possible

55
Q

At greatest risk TTTS

A
56
Q
A
56
Q

NRP - technique for compressions

A
57
Q

Delivery indications sPEC

A
58
Q

Mumps vs measles exposure pregnant woman - concerns

A
58
Q

Determine zygosity

A
59
Q

S/D

A
59
Q
A
60
Q

BPP components

A

BPP decision making

61
Q

PPROM and abx regimen

A
62
Q

Mat ACE - inhibitor

A
63
Q

Risk with mat MARFAN

A
64
Q

Which maternal med?

A
65
Q

Complications TTTS

A
66
Q

Oxygen transfer from placenta

A
67
Q

Complications to surviving twin of twin demise

A
68
Q

Complications mat epidural

A
69
Q
A
70
Q

Causes poly

A
71
Q

Risk factors Rh immunizaiton

A
72
Q

NRP question

A
73
Q

Benefits umb cord clamping

A
74
Q

Placenta in chorioamnionitis

A

Neo boards (14 decks)

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