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MMD1045: Module 2 > Embryo: Placenta > Flashcards

Embryo: Placenta Flashcards

1
Q

Décrit le développement du placenta lors de la semaine 2.

A

Ramification des villosités pénètrent l’endomètre plus profondément et leur architecture dendritique devient plus complexe

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2
Q

Décrit les villosités semaine 3.

A

Du mésenchyme apparait au centre des villosités
Des vaisseaux pénètrent le mésenchyme
Le mésenchyme est entouré de syncytiotrophoblastes

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3
Q

Comme quel organe agit le placenta pour le bebe

A

Poumons
Intestin
Rein

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4
Q

Est-ce que le sang foetal est en contact direct avec le sang maternel? Explique.

A

Le sang foetal n’entre pas en contact avec le sang maternel: ces deux circulations sont toujours séparées par les villosités trophoblastiques.

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5
Q

Separate mother vs fetus parts

Amnion
Vaisseaux
Chorion
Endomètre
Villosités
Cordon ombilical

A

Endomètre
Vaisseaux

Fetus:
Amnion
Chorion
Villosités
Cordon ombilical

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6
Q

À quoi sert le BHCG?

A

Stimule la sécrétion de progestérone par l’ovaire et évite lesmenstruation

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7
Q

Origine du chorion du placenta?

A

Extra-embryonnaire

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8
Q

Décrit l’endomètre suite à la sécrétion de progestérone.

A

Hypersécrétoire
Décidualisé
Devient la déciduale

Decidualization is a process that results in significant changes to cells of the endometrium in preparation for, and during, pregnancy

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9
Q

Décrit le développement des villosités placentaire.

A
  • Until the end of the 8th week, the entire surface of the amniotic membranes is surrounded by villi.
  • The growth of the embryo compresses the capsular villi, which become hypoxic and degenerate, while the villi closer to the cord insertion proliferate rapidly, widen, and branch like tree branches to form the placenta and increase the exchange surface with the maternal circulation.
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10
Q

Décrit le développement de l’espace intervillositaire.

A

Lacunes apparaissent dans le syntitio
Facteurs angiotrophes attirent les vaisseaux maternels
Fusion des lacunes: These cavities become confluent, eventually forming a single cavity of about 150 mL, the intervillous space, which is irrigated by 80 to 100 arterioles and countless endometrial venules.

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11
Q

What are primitive anchoring villi

A

The primitive anchoring villi (i.e., the first villi to appear at the level of the basal decidua) penetrate deeply into the endometrium to anchor the placenta in the uterus.

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12
Q

Décrit la formation de la couche de Nitabuch.

A

Villosités d’ancrage pénètrent dans l’endomètre et invasion du syntitio dans la déciduale

Nécrose de la déciduale en contact et formation d’une couche de fibrine, la couche de Nitabuch

The deep decidua becomes focally necrotic where it is in contact with the end of the villi, forming a layer of fibrin between the decidua and the syncytiotrophoblaste: the Nitabuch layer.

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13
Q

À quoi sert la couche de Nitabuch?

A

Nitabuch layer: This is what tells the villosities when they have grown enough, because if you grow more then you will enter the uterine myometer (muscle).

Chorionic villi cannot penetrate the Nitabuch layer; it is likely that this fibrin layer protects the embryo from maternal immunological rejection.

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14
Q

Qu’est-ce qui permet le flux sanguin turbulent dans l’espace intervillositaire?

A

Septas placentaire

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15
Q

Que sont les septas placentaires?

A

Projection de la déciduale

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16
Q

Qu’est-ce qui se passe avec le contact sang de maman/sang de bébé si les villosités choriales sont endommagés?

A

Il y a contact et les érythrocytes foetaux peuvent passer dans la circulation maternelle

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17
Q

How does the blood exchange change as the fetus grows?

A

When the baby is small there isn’t a huge need for nutriments and gas however, as it grows its energetic needs grow. The placenta cannot grow forever to increase its surface so instead it is the villosities (like in lungs) that multiply branches.

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18
Q

True or false:

that there is never an exchange of blood between the mother and the embryo only nutrient and gas.

A

True

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19
Q

How do you get child DNA in the mother?

A

trophoblast cells bathe in maternal blood; thus, when these cells detach from the villi, for example following their apoptosis, their DNA is released into the serum of the maternal blood.

This DNA can be analyzed for molecular karyotyping (e.g., for trisomy screening)

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20
Q

Comment les petites molécules traversent-elles la membrane placentaire?

A

Diffusion simple
Diffusion assisté
Transport actif
Pinocytose

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21
Q

Qu’est-ce qui se passe lors de l’accouchement d’une mère Rh- qui a un bébé Rh+?

A

If an expecting mother is Rh-negative and her baby is Rh-positive (by chance), the mother’s blood might produce anti-Rh antibodies.These antibodies can cross the placenta and damage the baby’s red blood cells, which could lead to life-threatening anemia.

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22
Q

Why is Rh- mother a problem even if first child survives? What is the solution?

A

Even if the current child survives, subsequent Rh+ pregnancies stimulate the mother to produce anti-Rh antibodies, now the mother is more prone to these. Antibodies cross the placental membrane and destroy the Rh+ erythrocytes of the fetus, causing hemolytic anemia

To avoid this complication, Rh- mothers are treated with anti-Rh antibodies within 72 hours after childbirth or abortion. These antibodies prevent the mothers’ immune system from reacting to Rh+ erythrocytes, as these antibodies destroy the Rh+ erythrocytes before they have time to stimulate an immune response in the mother.

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23
Q

Est-ce que les leucocytes de la mère peuvent migrer dans la circulation foetale?

A

The mother’s leukocytes (i.e., white blood cells) can migrate into the fetal circulation by diapedesis

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24
Q

Nomme les deux types de grossesses gémellaires.

A

Twin pregnancies can be of two types: monozygotic (identical) and dizygotic (fraternal twins).

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25
Q

Quand se produisent des jumeaux monozygotes?

A
  • Monozygotic twins are produced when a zygote abnormally divides to form two embryos;
    • these two embryos are genetically identical: they are clones.
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26
Q

Quand se produisent des jumeaux dizygote?

A
  • Dizygotic twins occur when the mother simultaneously produces two eggs that are fertilized by 2 different sperms to produce twins.
    • genetically different, of the same sex or not.
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27
Q

Que vont former deux morules qui se développent simultanément?

A
  • When two morulas develop simultaneously, either due to premature separation of blastomeres or a double ovulation, they form two independent blastocysts:
    • each blastocyst forms its own amnion and its own amniotic cavity, each surrounded by a layer of trophoblast that produces its chorion.
28
Q

Can a fused placenta tell us that we have a monozygotic pregnancy?

A

Nope
When two morulas develop simultaneously,- If these two blastocysts implant far from each other, their placentas will not be fused; if they implant closer, their placentas will be fused.

  • Regardless, the dividing membrane (i.e., the leaflet delimited by the apposition of the amniotic membranes) will have four layers of tissue.

placenta di-di can be for identical OR fraternal twins!!

29
Q

Décrit la membrane mitoyenne de deux morulas. (di-di)

A

amnion - chorion - chorion - amnion, hence the term diamniotic-dichorionic placenta.

30
Q

True or False,

Di-Di twins will have independent circulations.

A

True

31
Q

Décrit le placenta DiMo.

A

Deux cavités amniotiques
Un placenta

32
Q

What can tell us that the twins are identical?

A

Ce n’est que lorsque le placenta est mono-chorionique (DI-MO or MO-MO) que l’on peut dire que les** jumeaux sont identiques**; dans les cas où le placenta est di-chorionique avec des jumeaux de même sexe, on ne peut dire s ‘ils sont identiques ou fraternels.

33
Q

Vrai ou faux? Les placentas MoMo sont toujours monozygotique.

A

Vrai

34
Q

Décrit la formation des jumeaux siamois

A

Bouton embryonnaire ne se scinde (divides) pas complètement

Deux lignes primitives dans le même embryon

Exceptionally, in cases when the embryonic bud does not split completely, or two primitive streaks develop within the same embryo, we can have the forming of conjoined twins.

Conjoined twins,popularly referred to as Siamese twins, are twins joined in utero

35
Q

In what type of pregnancy is there shared blood circulation between the twins?

A

DI-DI and MO-MO twins have independent circulations.

However, in DI-MO there is a vascular exchange between the two babies.

36
Q

DI-MO there is a vascular exchange between the two babies

What is the issue?

A

pregnancies are at risk of developing a transfusion-transfused syndrome (TTS).

  • In most monochorionic pregnancies, the blood exchange between the twins is balanced. However, in about 10% of these pregnancies, the blood exchange is unequal, leading to TTS.
    • This leads to differences in pressure which can then lead to imbalanced blood flow.
  • This happens when the blood flow is uneven and passes from one twin (the donor) to the other (the recipient)
  • The donor twin gives more blood than it receives, leading to dehydration, decrease in amniotic fluid. The recipient twin receives too much blood, leading to an increase in amniotic fluid.
  • Can eventually cause heart failure and death in one or both fetuses

pregnancies where two twins share a single placenta, known as “monochorionic”

37
Q

Qu’est-ce que la chorioamnionite?

A

ite- Infection or inflamation

  • Ascending infection caused by bacteria that move from the vagina to the membranes via the cervix.
  • These infections often cause premature rupture of the membranes, leading to premature birth.
    • The bacteria proliferate in the amniotic fluid. The fetus, which breathes this fluid, is at risk of developing pneumonia → death.
    • Better to abort than lead to death + mother infection.
38
Q

Traitement d’une chorioamnionite?

A

Fait sortir le bébé rapidement

39
Q

Impact d’une chorioamnionite sur le cerveau du foetus?

A

Cerveau prématuré et paralysie cérébrale:

Le cerveau des prématurés est très sensible aux cytokines produites lors de la réaction inflammatoire associée à la chorioamnionite;

Cytokines peuvent causer une nécrose de régions cérébrales motrices, particulièrement lorsqu’il y a une hypoxie associée.

Again, only motor problems without intellectual damage.

Only touches white matter and not gray matter.

The facial motor region is only slightly affected

40
Q

Describe Placental infarction:

A

Cocaine and maternal thrombophilias (which can cause a hypercoagulability syndrome) predispose to the development of intervillous thromboses (blood clots that form between the villi, preventing normal irrigation of the maternal circulation around the involved villi), with placental necrosis

Complications related to fetal hypoxia are more severe when these thrombi form early in pregnancy, and are proportional to the extent of the thrombosis

Hypercoagulation is more severe in homozygous mutations and when more than one of these genes is mutated.

41
Q

Localisation des hématomes rétroplacentaires?

A

Hematomas are located between the placenta and the uterus.

42
Q

Conséquences and causes of hématomes rétroplacentaires?

A

Relatively common and often associated with intrauterine death (IUD).

Can be caused by chorioamnionitis, maternal hypertension, and maternal hypercoagulability syndrome.

43
Q

Que cause l’hypertension maternelle?

A

Causes placental infarctions (areas of tissue death due to lack of blood flow or oxygen).

This results in the fetus getting less oxygen, leading to intrauterine growth retardation (RCIU) which can be severe.

Considering the intrauterine circulation, the head gets more oxygen than the trunk and limbs. This results in an asymmetric RCIU: the head is relatively larger than the body.

An RCIU caused by genetic reasons is usually symmetric (opposite of what we have here)

44
Q

What is the difference of the maternal hypertension related RCIU vs genetic?

A

In hypertension: asymmetric RCIU: the head is relatively larger than the body.

An RCIU caused by genetic reasons is usually symmetric

45
Q

Qu’est-ce que la pré-éclampsie?

A

Severe form of hypertension present prior to pregnancy or caused by pregnancy.

Associated with proteinuria (secondary to hypertensive glomerular lesions of the baby with baby’s proteins getting in mother’s urine) and significant edema (secondary to hypoalbuminemia)

46
Q

En quoi peut évoluer une pré-éclampsie? What is the treatment?

A

Pre-eclampsia can progress into eclampsia, which is pre-eclampsia complicated by maternal epilepsy, usually fatal

The only effective treatment to prevent eclampsia is delivery, which must be done quickly, at the latest a few days after the onset of symptoms.

Accouchement rapide

47
Q

Qu’est-ce qui prédispose à l’infarcissement placentaire?

A

Cocaine
Trombophilies

48
Q

Vrai ou faux? Les complications liés à l’hypoxie foetale sont moins sévères quand le thrombi se forme tôt

A

Faux

49
Q

Décrit une hypercoagulation sévère.

A

Mutation homozygote
Multiples mutations

50
Q

Conséquence du syndrome du cordon long?

A

Pression de la veine ombilicale faible
Strangulation
Formation de noeuds

  • When the tension increases at a knot or a loop around the neck, the fetoplacental circulation is compromised and can cause intrauterine death (IUD).
  • This can either be under high pressure, or not.
  • Important to note that the venous return will have lower pressure and thus a harder time getting back to the mother.
51
Q

True or False

Le syndrome du cordon court est commun

A

False

This pathology is very rare.

52
Q

Conséquences du syndrome du cordon court?

A

causes traction on the abdominal skin and on the amnion

  • The traction on the amnion can tear it, and if this amnion separates from the chorion it can wrap around the skull, trunk, limbs, and fingers, causing amputations or clefts
  • If the fetus swallows these amniotic bands, they can tear the lips, cheeks, and jaw.
53
Q

True or false

Les fentes engendrés par le syndrome du cordon court sont des malformations

A

Non, ce sont des déformations

54
Q

Qu’est-ce qui a un plus grand risque de récidive, malformations ou déformations?

A

Malformations

55
Q

Qu’est-ce qui cause une exsanguination maternelle?

A
  • In cases of placental abruption, the chorionic villi can tear.
  • The arterial pressure of the fetal villi can be higher than the venous pressure of the maternal intervillous vascular spaces.
  • In these cases, the fetus’s blood can spill into the maternal circulation, leading to the death of the fetus by exsanguination.
  • These fetuses are generally very pale.
56
Q

Effet de l’exsanguination maternelle?

A

Sang du foetus se déverse dans la maman
Mort du foetus
Très pâle

57
Q

What is Kleihauer-Betke test.

A

Test pour vérifier l’exsanguination maternelle

  • Fetal blood is more resistant to hypotonic shock than adult blood.
  • A hypotonic shock is applied to maternal blood.
  • If there is no more blood left, then there was no fetal blood in the circulation.
  • If there is blood, that is because some of the fetus blood was circulating in the mother.

  • The number of non-lysed erythrocytes (fetal erythrocytes) remaining in this maternal blood is evaluated to determine if there is fetal blood.
58
Q

When can transfusion-transfused syndrome (TTS) occur?

A

an occur in pregnancies where two twins share a single placenta, known as “monochorionic” pregnancies.

59
Q

Est-ce que le syndrome de transmission gémellaire est commun pour les jumeaux MoMo?

A

False

Only occurs in Di-Mo

DI-DI and MO-MO twins have independent circulations.

However, in DI-MO there is a vascular exchange between the two babies.

60
Q

Que sont les chorangiomes?

A

Tumor of the villosité chorial (placentaire)

pas d’impact clinique lorsqu’ils sont petits

les chorangiomes volumineux causent un shunt et peuvent occasionner une défaillance cardiaque:

le coeur ne peut pas pomper suffisamment pour irriguer le chorangiome et les autres tissus.

61
Q

Que sont les placenta accreta, increta et percreta?

A

Anomalies du placenta qui infiltrent le myomètre superficiel, le myomètre jusqu’à la séreuse de l’utérus

Caused by an anomaly of the basal decidua, which normally generates a layer of fibrin: the Nitabuch layer.

The formation of this layer is essential to prevent the invasion of the decidua and the muscular wall of the uterus (myometrium) by the villi. (seen earlier)

62
Q

Cause des placenta accreta, increta et percreta?

A

Caused by an anomaly of the basal decidua, which normally generates a layer of fibrin: the Nitabuch layer.

The formation of this layer is essential to prevent the invasion of the decidua and the muscular wall of the uterus (myometrium) by the villi. (seen earlier)

63
Q

Qu’est-ce qui se passe quand les villosités infiltrent le myomètre?

A

When the villi infiltrate the myometrium, the placenta does not detach from the uterus, which prevents the contraction of the uterus and can lead to exsanguination by massive hemorrhage.

64
Q

Traitement du placenta accreta, increta et percreta?

A

An emergency hysterectomy (resection of the uterus) may be required to prevent the death of the mother

65
Q

Décrit l’aspiration de méconium.

A

Acute hypoxia in the fetus stimulates two reflexes: a contraction of the rectum with dilation of the anus and a deep aspiration.

The fetus then inhales a more or less significant amount of meconium (fecal matter in the rectum of the fetus)

  • This intra-alveolar meconium destroys the surfactant, which can significantly disrupt the expansion of the alveoli and their gas exchanges → lung malformation.
66
Q

Qu’est-ce que l’insertion vélamenteuse du cordon?

A

Insertion of the cord into the membranes rather than directly above the placental disc.

Velamentous insertion is generally without clinical impact.

Rarely, the “normal” rupture of the membranes during childbirth can tear the associated vessel, causing a sudden hemorrhage of the fetus, which is often fatal.

67
Q

Qu’est-ce que le méconium?

A

Matière fécale du foetus

MMD1045: Module 2 (11 decks)

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