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Disorders of pregnancy and parturition Flashcards

1
Q

What type of nutrition is present in the early embryos?

A

Histiotrophic nutrition

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2
Q

Describe Histiotrophic nutrition

A

Syncytiotrophoblast breakdown of endometrial tissue and uterine gland secretions provide nutrition
histio - tissue
trophic - feeding/growth
growth with tissue as the source of energy

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3
Q

What type of nutrition is present in the second trimester?

A

Hemotrophic (more chorionic villi)

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4
Q

Describe Hemotrophic nutrition

A

Nutrients delivered to placenta via maternal blood

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5
Q

What is a hemochorial type placenta

A

maternal blood directly contacts the fetal membranes
(chorionic villi)

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6
Q

How do fetal demands on the placenta change with time

A

Increased demands as the pregnancy progresses

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7
Q

How does the placenta change through pregnancy?

A

Chorionic villi become increasingly branched to allow a greater surface area for nutrient exchange.

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8
Q

How is the placenta structured

A

Fetal artery and vein (umbilical cord) branches into chorionic villi which are bathed in maternal blood, within the lacunae (maternal blood space). These lacunae are supplied by spiral arteries.

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9
Q

What are chorionic villi

A

finger-like extensions of the chorionic cytotrophoblast

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10
Q

What are the three phases of chorionic villi development?

A

Primary - outgrowth of cytotrophoblast + branching
Secondary - growth of fetal mesoderm into villi
Tertiary - umbilic artery & vein grows into fetal mesoderm which is now in villi

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11
Q

What is the structural adaptation of terminal villi to allow blood exchange?

A

Takes the appearance of a convoluted knot of vessels
This slows the blood and allows more time for exchange
Diameter thins over time, which provides a short diffusion pathway

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12
Q

What happens to spiral arteries as pregnancy progresses?

A

Spiral artery remodelling

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13
Q

What is spiral artery conversion

A

Artery becomes low pressure, high capacity conduit for maternal blood flow

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14
Q

what are EVT

A

Extra-villus trophoblast cells, coat the chorionic villi

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15
Q

Describe the process of spiral artery remodelling

A

EVT invade spiral arteries forming endovascular EVT
Triggers endothelium activation and recruitment of chemoattractants and .: WBC
WBC breaks down endothelium and smooth muscle
Endo EVT causes ECM to be replaced by fibrinoid

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16
Q

What happens if spinal artery remodelling fails?

A

smooth muscle remains
WBC are embedded in the vessel wall - proinflammatory environment
Occlusion of the artery occurs due to lack of space

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17
Q

What pathological change are unconverted spiral arteries at risk of

A

Atherosis - fat buildup
Intimal Hyperplasia - Extra wall cells

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18
Q

Consequences of failed spinal artery remodelling

A

Retained smooth muscle allows contraction -> Perturbed blood flow -> local hypoxia
free radical damage -> apoptosis
inefficient delivery of substrates to the intervillous space

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19
Q

What is preeclampsia

A

New onset hypertension post 20wks gestation (>140/90)
associated with proteinuria

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20
Q

What are the common symptoms of pre-eclampsia?

A

Reduced Fetal Movements, Reduced Amniotic Fluid, Oedema, Headache/Visual Disturbances, Abdo Pain, Eclampsia

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21
Q

What is eclampsia?

A

Seizures

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22
Q

What are the subtypes of pre-eclampsia?

A

Early Onset (20-34 weeks)
- Both fetal + maternal symptoms
- changes in placenta structure
- red placenta perfusion

Late Onset (>34 weeks)
- maternal symptoms only
- No changes to placenta structure

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23
Q

What are the risks to the mother in pre-eclampsia?

A

Organ Damage, (endothelial damage and death of glomerular cells)
Eclampsia,
HELLP Syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets)
Placental abruption (sep from endometrium)

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24
Q

What are the risks to the fetus in pre-eclampsia?

A

Pre-term delivery,
Intra-uterine growth restriction, (fetal growth restric)
Fetal death

25
What are the defects to spinal artery remodelling in pre-eclampsia?
EVT do not travel deep enough, stop at decidua b4 myometrium Spiral arteries remain spiralled higher up leading to less blood flow and hence less placental perfusion
26
What growth factors are released by the placenta?
PLGF (Placental Growth Factor) VEGF (Vascular Endothelial Growth Factor) They are both Pro-angiogenic + vasodilatory
27
Receptor that binds PLGF/VEGF
Flt1 soluble receptor binds soluble angiogenic factors to limit their bioavailability
28
How does PE affect the action of PLGF/VEGF
Distressed placenta produces more Flt1 which binds to these growth factors and reduces their bioavailability in maternal circulation. Lack of signals causes endothelial dysfunction (procoagulants and vasoconstriction)
29
What are extracellular vesicles
tiny lipid bilayer laminated vesicles released by almost all cell types. contain lipids, proteins and nucleic acids - can influence cell behaviour both locally and at a distance.
30
Role of extracellular vesicles
Released by donor cells to act on target i.e. cell signalling autocrine, act on donor cells paracrine, act on other cells endocrine, dif tissues/organ
31
Preeclampsia impact on extracellular vesicles
Increase in EV in maternal circ Increase in endothelial derived EV (debris from damaged mother's endothelial cells - due to dysfunction) Decrease in placenta derived EVs (different signals to normotensive placenta)
32
Proposed mechanism behind PE
SDEV (syncytiotrophoblast derived extracellular vesicles), released due to placenta ischaemia and trophoblast apoptosis Contain the wrong cargo (flt1, endothelin, TNFa, IL) Induces endothelial dysfunction, inflammation and coagulation disorders -> preeclampsia
33
What is the cause of later onset pre-eclampsia?
Not understood yet suggested theory: women with genetic CVD risk manifest symptoms bc of pregnancy stress
34
Timeline of PE development
Genetic factors (SNPs), Maternal/Environmental factors (smoking, DM, AKI) and Immunological factors (xtra WBC) -> abnormal placentation (superficial invasion) -> Placental ischaemia, oxidative stress, persistent hypoxia -> ^ circulating sflt1 (^ EV and pro-inflam cytokines) -> systemic vascular dysfunction -> PE symptoms Proteinuria, Hypertension, HELLP syndrome, Visual disturbances, Eclampsia May lead to a small for gestational age infant
35
What is the consequence of placental ischaemia?
Fetal Growth Restriction (same as intra-uterine GR)
36
What are the two stages of pre-eclampsia development?
Stage 1 (Abnormal Placentation) // Stage 2 (Maternal Syndrome)
37
What are the factors that lead to stage 1?
Genetic (increased sFlt1 genes) // Environment (ckd, t2dm, htn) // Immunological
38
What is the consequence of systemic vascular dysfunction in pre-eclampsia?
Proteinuria, Hypertension, Headache/Visual Disturbances , HELLP Syndrome, Eclampsia
39
What are the two measurements that can be used to detect pre-eclampsia?
PLGF Levels (<100 is abnormal), high sensitivity and red diagnosis time sFlt-1 : PLGF ratio (>38 is abnormal)
40
Issues with PLGF/ sFlt1:PLGF
Not definitive Cannot predict PE b4 onset. only useful post 20wks
41
Future PE diagnosis methods
Examine cfRNA (cell free) from maternal blood Examine small molecule metabolites in urine to reveal biosignatures
42
What is SGA?
Small for Gestational Age - baby is < 10th centile
43
What is severe SGA?
Baby is < 3rd centile
44
What are the three subclassifications of SGA?
Small throughout pregnancy but healthy Early growth is normal, slows later in pregnancy (IUGR/FGR) Non-placental growth restriction (genes, metabolism, infection)
45
What is the difference between SGA and IUGR?
SGA is only fetal weight without considering growth patterns IUGR assesses signs of malnutrition irrespective of fetal weight (therefore a baby can be IUGR without SGA and vice versa)
46
What are the two types of IUGR?
Symmetric, Asymmetric
47
What are the difference in growth reduction patterns between asymmetric/symmetric IUGR?
Symmetric has a proportional reduction in growth Asymmetric is head&brain sparing - normal head shape but smaller abdomen and torso
48
What is the relative difference in cell number and cell size between the the two types of IUGR?
Symmetric - Low cell number normal size Asymmetric - Normal number low cell size
49
Which of the two have a poorer prognosis? Symmetric vs Asymmetric IUGR
Symmetric IGUR also the rarer form
50
Aetiology of asymmetric IUGR
Utero-placental insufficiency Placenta cannot provide sufficient nutrients and development favours the brain More pronounced features of malnutrition
51
Aetiology of symmetric IUGR
Genetic disorder Infection
52
What 3 systems are implicated by IUGR
Cardio, Resp, Neuro
53
How does IUGR affect the cardio system
cardiac hypertrophy, vasoconstriction -> remodelling of fetal vessels
54
How does IUGR affect the Resp system
bronchopulmonary dysplasia, immature lungs
55
How does IUGR affect the Neuro system
motor defects, cognitive impairments
56
What are the two mechanisms of IUGR?
Villous Maldevelopment, (genetics) Vascular Malperfusion (defect with EVT invasion)
57
What is villous maldevelopment?
Villi do not form properly - impaired blood exchange - fetal impoverishment
58
What is vascular malperfusion?
placental bed pathology -> blood supply does not perfuse through the placenta as it should
59
What other condition is caused by vascular malperfusion?
Early Onset Pre-Eclampsia

Dev/Age (4 decks)

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