Sept11 M1-Perinatal Pathology Flashcards

1
Q

fetus and mother relationship

A
  • uterine wall (implant high up to avoid rupture on delivery)
  • placenta with maternal surface and fetal surface
  • fetal surface (linked to placenta with amniotic cord)
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2
Q

appropriate size of placenta for gestational age def

A

each age has an ideal size to weight ratio and this ratio changes with age

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3
Q

(imp) 4 components of placenta

A
  • fetal membranes (amnion and chorion)
  • umb cord
  • trophoblastic villi
  • retro-placental decidua and vessels
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4
Q

fetal membrane def

A

wraps around fetus and extends on placental surface

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5
Q

trophoblastic villi def

A

where O2 and nutrients transfer occurs. the maternal vessels supply these villi

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6
Q

retro-placental decidua and vessels def

A

the retroplacental surface has decidua and vessels

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7
Q

fetal surface of placenta blood supply

A
  • umb cord on top (fetal surface)
  • ramifications into cotyledons (stems of trees)
  • stem villus (main branch of cotyledon)
  • villous tree, trophoblastic villi (other branches of cotyledon)
  • intervillous spaces filled with RBCs of the mom
  • decidua in bottom (maternal vessels, side)
  • so RBCs will swim in branches then cotyledons then cord*
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8
Q

fetal surface of placenta 2 surfaces on top

A
  1. amnion
  2. chorion below it
    * are where this blood exchange is happening
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9
Q

how many cotyledons for how many villous trees

A

each cotyledon gives one villous tree

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10
Q

cells in trophoblastic villi

A
  • cytotrophoblasts (gives rise to syncytiotrophoblasts)
  • syncytiotrophoblasts
  • syncytio = final differentiation for exchange through capillaries
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11
Q

fetal capillaries are considered to be where in the placenta

A

are the trophoblastic villi (bc will receive RBCs from mother that are outside)

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12
Q

villi cells behavior and why

A

group together so thinner BM so more exchange

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13
Q

decidua component

A

maternal vessels and intermediate trophoblasts

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14
Q

1st step of delivery

A

rupture of membrane surrounding fetus and spreading around placenta

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15
Q

extra-placental fetal membranes def

A

limit between rupture site (of membrane) and edge of placenta

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16
Q

relevance of rupture site clinically

A

infection often there if rupture too early. first there and then spreads up to placental cells

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17
Q

how membranes prepared for path

A

make a roll with it starting at the rupture site (most internal) so external part of roll is most external

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18
Q

inflammation more in center of membrane roll meaning

A

early infection

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19
Q

inflammation in whole membrane roll def

A

infection from >24 hours

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20
Q

normal nbr of vessels in umb cord

A

3

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21
Q

what if cord has 2 vessels

A

possible malformations

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22
Q

how to see if blood flow obstruction in placenta

A

check if change in color

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23
Q

variations in placental shape (normal = oval)

A
  • bilobed (because of a true knot in cord)
  • accessory lobe (lobe that goes away from main chorionic plate. prob = goes near internal os and membrane fragile, can rupture vessels)
  • circumvallate (vessels don’t go to the edge of the placenta, membrane goes around and forms a ring around it. prob = possible hemorrhage at wall of membrane, margin at time of delivery)
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24
Q

green placenta reason

A

passed meconium. either

  • premature baby that passed meconium which stained the membrane
  • sign of fetal stress (hypoxia, less O2, less sphincter control)
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25
Q

anomalus insertions of the umb cord

A
  • marginal, at edge of chorionic plate

- velamentous, outside chorionic plate

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26
Q

velamentous insertion charact

A

out in extra placental membrane away from placenta, vesses have to travel, can be precarious (unsafe, dangerous)

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27
Q

condition for bacteria to infect placenta and exception

A

membrane has to rupture

-except beta hemolytic strep, can get through if intact

28
Q

most common way of infection (bacteria)

A
  • trans cervical amniotic region has a ruptured membrane

- infection comes from vagina

29
Q

common bacteria for placental infection

A
  • e coli (gram - enteric bacteriae)
  • anaerobes
  • beta strep if non ruptured
30
Q

what infection can do once in placenta

A

can reach the fetus

31
Q

2 ways of infections of the placenta and fetus + name of the infection

A
  1. hematogenous (from mother blood, for ex CMV). called VILLITIS
  2. ascending infection (most common, ruptured memb near cervix, inf ascends form vagina) called CHORIONITIS OR CHORIO-AMNIONITIS
32
Q

how to suspect infection at delivery

A

cloudy fetal surface, not clear fetal surface of placenta

33
Q

thing for biggest suspicion of infection other than cloud surface

A

premature ruptured membranes (2 days before delivery)

34
Q

chorionitis or chorioamnionitis on histo

A

inflam infiltrate through chorion or both chorion and amnion (those are on fetal side)

35
Q

funisits def

A
  • infection of chorion and amnion extends into Wharton’S jelly (mesenchymal substance arround tree vessels giving them bouncy stability) of the cord
  • vasculitis of cord vessels
36
Q

how to detect funisits on histo

A

inflammatory infitlrate extends from amnion and chorion to Wharton’s Jelly

37
Q

order of infection in a funisitis

A
  1. infection spreads from amnion and chorion to a vein and get vasculitis in a VEIN
  2. funisitis
  3. infection spreads from Wharton’s jelly to artery = get vasculitis in an ARTERY
38
Q

signs of vasculitis in cord infection

A

inflammation + polymorphs (polymorphonuclear neutrophils)

39
Q

what fetus does during infection

A

keeps swallowing and urinating and passing feces as usual so infection can end up in the lung

40
Q

first sign of intra-fetal infection

A

pneumonitis = infection in the lung (peribronchiolar inflammatory infiltrates)

41
Q

causes of hematogenous infections of placenta and fetus

A
  • TORCH group (toxoplasma, rubella, CMV, herpes simplex)

- parvovirus

42
Q

sign of parvovirus infection in the fetus

A

fetal hydrops

  • edema in the fetus
  • cause = virus attacks hemopoietic system of fetus so gets anemic and heart works harder)
43
Q

how to see parvovirus infection of placenta and fetus on histo

A
  • intervillositis (inflam in intervillous spaces)
  • maternal polymorphs in intervillous space
  • villitis eventually if extends in villi
44
Q

how to see CMV infection of placenta and fetus on histo

A
  • big inclusions of CMV

- lymphocytes in villi (NOT polymorphs, meaning no neutrophils)

45
Q

order of arteries to reach decidua (or top of endometrium, normally, in non pregnant woman)

A
  • uterine a (vertical)
  • arcuate a (horizontal)
  • radial a (vertical))
  • spiral aa (continuation of radial a, vertical)
  • basal aa (branches of spiral aa)
46
Q

spiral aa normal reaction to pregnancy

A

dilate to accomodate blood to placenta

47
Q

pre-eclampsia prob

A

spiral aa don’t dilate and remain thick walled and narrow

-placenta poorly perfused

48
Q

signs of pre-eclampsia, thickened maternal vessels on histo (and progression with severity)

A
  1. hypertrophic vessels in the decidua of placenta
  2. subintimal degenerative changes (accum of fat laden macrophages under the intima)
    AND perivascular lymphocytes
  3. vasculopathy (fibrinoid replacement of intima)
49
Q

thickened vessels on macroscopy how to see

A

see an amount of marginal blood clots and blood in the placenta that is abnormal (ruptured vessels and clots (in excess). marginal blood clots is normal but too blood in placenta is abnormal.

50
Q

abruptio placentae def

A
  • retro-placental bleed
  • bleed covering whole maternal surface now and not just margins
  • elevation of a bed of clots over whole maternal surface
  • still related to thickened vessels*
51
Q

possible consequence of placental decidua vessels rupture or thrombosis

A
  • villi are infarcted (collapse and undergo changes bc of vascular obstruction)
  • villi eventually necrotic
52
Q

how to recognize villous infarctions on placenta

A
  • very dark, not red

- placenta firm not spongy

53
Q

other name of villous infarctions

A

infarction of maternal vessels

54
Q

when can villous infarction cause fetal damage

A

if extended over more than 30% of thickness of placenta

55
Q

histo of hematomas (blood clots) on side of villous infarction during maternal vessel infarction shows what

A

crevisses

56
Q

etiologies of fetal asphyxia

A
  • placental pathology (e.g. abruptio placentae)
  • cord accidents (a problematic true knot (not always prob), anomalous insertion with rupture, thrombosis
  • sepsis (GBS with endotoxic shock)
57
Q

cause of asphyxia in sepsis and endotoxic shock

A

endothelial damage

58
Q

non problematic true knot

A

all same color and red

59
Q

true knot with thrombosis, causing fetal demise

A

change in color. red to pale

60
Q

main way of detecting asphyxia in the fetus

A
  • petechiae hemorrhages on serosal surfaces (chest organs, etc.)
  • more severe asphyxia = periventricular hemorrhage in the brain (can cause cerebral palsy)
61
Q

intra-uterine growth restriction def

A

perinatal pathology where the baby is small for gestational age, also called small baby

62
Q

small baby determined how

A

by checking size to weight ratio after delivery and check if is right for gestational age

63
Q

causes of small baby

A
  • constitutional (small placenta) (asymmetric)
  • placental insufficiency (deficient maternal blood flow. will see mature villi (38 weeks) at week 34 for ex bc tried to accomodate and mature) (asymmetric)
  • malformation syndromes (trisomies, etc.) (asymmetric)
  • social habits (SMOKING is the main one. drugs, etc.) (asymmetric)
  • congenital infections of TORCH group during T1. called symmetric smallness bc caused early and stay small throughout pregnancy.
64
Q

cocaine used assoc with what perinatal pathology

A

abruptio placentae

65
Q

causes of intrauterine fetal deaths (stillbirths)

A

-placental insufficiency
-asphyxia
-infection
malformation syndromes (can be assoc with maternal disease like pre-eclampsia so don’t rule out placental causes important**)
-others