Placenta Flashcards

(38 cards)

1
Q

Which cell type in placenta secretes hormones?

A

Trophopblast

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2
Q

Trophoblasts secrete what?

A

growth factors, immuno modulators, sex steroids, metabolic mediators (leptin, lactogen), neuromodulators (CRF and seratonin)

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3
Q

Placenta has receptors for what hormones?

A

glucocorticoids, insulin, insulin like growth factors, leptin, gonadal hormones, cytokines, prostaglandins

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4
Q

One big difference between human v rat placenta?

A

synthesis of estrogen

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5
Q

placentas can be classified as

A

epitheliochorial, endotheliochorial, hemochorial (based on which of mother’s cells contact fetal trophoblast)

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6
Q

Blood route in placenta

A

maternal blood enters the placenta from the uterus through the myometrium into the metrial gland, crosses the decidua, reaches the labyrinth layer, drains via the venous sinuses traversing the junctional zone into the decidua and exits via the metrial gland and the myometrium to the uterus

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7
Q

functions of placenta

A

(1) to ensure delivery of maternal nutrients and blood gas (O2 and CO2) to the placenta, (2) to transfer nutrient and oxygen from the placenta to the developing fetus, (3) to produce hormones and growth factors, and (4) to protect the developing fetus against infections

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8
Q

main components of rat placenta

A

decidua /metrial gland (maternal origin)
yolk sac, amnion membranes, basal zone (junctional zone)
labryinth and junctional zone (fetal, basal zone)

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9
Q

Trophoblast (consists of cytotrophoblast, syncytiotrophoblast) describe each

A

cyto: slowing the maternal blood,
sync: Main site of exchange,form a layer that separates fetal and maternal circulation

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10
Q

junctional zone function

A

production of steroids and peptide hormones
Spongiotrophoblast
Main structural component of the basal zone
Trophoblastic giant cells They are below the spongiotrophoblast layer, Phagocytic activity to mediate implantation, Major endocrine cell of the placenta
Glycogen cells

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11
Q

decidua function

A

decidual stromal cells
produce pro- and anti- inflammatory cytokines, immune cells, growth factors and hormones

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12
Q

commonalities/diff between rat and human placenta

A

discoid in shape, hemochorial

differing names of structure: labryinth vs placental villi
basal zone v basal plate
labryinth v villous
rat placenta absence of aromatase !

rat is antimesometrial

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13
Q

histological stages of human chorioamnionitis

A

Stage 1: lesion characterized by presence of neutrophils in the chorion or subchorionic space
Stage 2: a cluster of microabscessesneutrophilic infiltration of the chorionic connective tissue and/or amnion or chorionic plate
Stage 3: necrotizing chorioamnionitis with degenerating neutrophils

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14
Q

What % of cells make up the leukocytes in chorioamnionitis?

A

60% neutrophils
10% macrophage
15% t cells

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15
Q

neutrophils employ what in their defense?

A

NETs, ROS, antimicrobial enzymes, defensins, neutrophil elastase, myeloperoxidase

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16
Q

Whats in the labyrinth?

A

trophoblast (cytotrophoblast, cyncitiotrophoblast)

17
Q

What’s in the junctional zone?

A

spongio trophoblast, glycogen cells, trophoblastic giant cells

18
Q

do fetal capillaries penetrate into the JZ?

19
Q

PMNs have three important antimicrobial functions:

A

phagocytosis, degranulation, and the release of material via neutrophil extracellular traps composed mainly of DNA from neutrophils trapping pathogens

20
Q

major diff bw rat and placenta?

A

human more invasive: with only one layer of trophoblast separating the maternal blood from fetal endothelial cells as compared to three layers in rodents

21
Q

What is sterile inflammation in the context of pregnancy?

A

Sterile inflammation refers to an immune response characterized by activation of inflammatory pathways in the absence of viable microbial infection. It can be induced by exposure to pathogen-associated molecular patterns (PAMPs) from inactive or non-replicating bacteria, such as heat-killed Group B Streptococcus (GBS), leading to placental dysfunction and adverse pregnancy outcomes.

22
Q

Why are pregnant women more susceptible to infections

A
  1. Immune system modulation
    Pregnancy doesn’t suppress the immune system—it modulates it:

The immune system shifts to tolerate the fetus (which is genetically half foreign).
There is a tilt toward anti-inflammatory responses in early and mid-pregnancy (to allow implantation and growth), followed by a pro-inflammatory phase in late pregnancy (to prepare for labor).

  1. Hormonal changes
    Increased levels of progesterone and estrogen can alter immune responses and mucosal barrier integrity, sometimes reducing local defenses.
23
Q

why is Group B Streptococcus (GBS) screening performed between 35-37 weeks of gestation?

A

The GBS screening swab is performed between 35-37 weeks because colonization status can fluctuate during pregnancy, and screening close to delivery provides the most accurate prediction of neonatal exposure risk, allowing timely intrapartum antibiotic prophylaxis to prevent early-onset neonatal GBS disease.

24
Q

How does GBS activate the NF-κB pathway in placental cells?

A

Through TLR recognition of bacterial components, triggering downstream signaling cascades that activate NF-κB and promote proinflammatory cytokine production.

25
How can GBS impact the fetal brain without translocating across the placenta?
Likely via inflammatory mediators (e.g., cytokines, chemokines, or EVs) that cross into fetal circulation and brain tissue, contributing to MIA-driven neuroinflammation
26
How might a viral pathogen trigger MIA differently than GBS?
Viral PAMPs typically activate different TLRs (e.g., TLR3, TLR7) and may induce type I interferons more robustly, leading to a distinct cytokine profile and immune response.
27
How might a viral pathogen trigger MIA differently than GBS?
Viral PAMPs typically activate different TLRs (e.g., TLR3, TLR7) and may induce type I interferons more robustly, leading to a distinct cytokine profile and immune response.
28
Why is intrapartum antibiotic prophylaxis insufficient for GBS-induced MIA?
It’s given at delivery and doesn’t address early inflammatory events or chorioamnionitis occurring well before labor.
29
What defines the different strains of GBS? Why is this relevant?
GBS strains are classified by the structure of their capsular polysaccharides, which are important for immune evasion. Serotype Ia: Found in 25–50% of human perinatal infections Serotype III: Found in 10–25% These serotypes have different capacities to colonize and induce inflammation
30
How does GBS persist in the vaginal tract despite immune surveillance?
GBS uses invasion and defense strategies (e.g., molecular mimicry, immune evasion proteins) that allow it to remain a natural part of vaginal flora—often undetected unless host immunity is altered (Patras and Nizet 2018).
31
What are the two main pathways through which GBS activates innate immunity?
PAMP-TLR pathway: GBS components like lipoteichoic acid, peptidoglycan, and β-hemolysin are recognized by Toll-like receptors (TLRs), especially TLR2 and TLR4, initiating cytokine release.
32
in fetus during pregnancy high cortisol means what for androgen?
high androgen but in adults high cortisol = low androgen
33
What is a Capsular Polysaccharide (CPS)?
Capsular polysaccharide (CPS) is a sugar-based outer coating that surrounds certain bacteria, including Group B Streptococcus (GBS). The CPS is a key virulence factor — it helps GBS evade the host’s immune system. many serotypes:which vary in virulence
34
Why not look at macrophages?
The number of CD68+ or Iba-1+ macrophages was identical in GBS-exposed and control placental labyrinths (data not shown). (2013) Meanwhile...Focal or diffuse decidual PMN infiltration was observed in 75% of GBS-exposed placentas
35
Are NETs good?
Double edged sword, contain pathogen but also damage tissue and fuel inflammation
36
what does linear calcification and inc placenta weight mean?
calc: abnormal calcium deposits in tissue, patterned or structured deposition, often indicating chronic inflammation A heavier placenta is often a sign of inflammation, edema, or immune cell infiltration This ratio is a key measure of placental efficiency. A lower ratio means the fetus is getting less growth per gram of placenta, suggesting placental dysfunction.
37
37
what about structure and architecture of placenta?
disrupted villous structure