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Dev/Age > Disorders of pregnancy and parturition > Flashcards

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
Q

What are the defects to spinal artery remodelling in pre-eclampsia?

A

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
Q

What growth factors are released by the placenta?

A

PLGF (Placental Growth Factor)
VEGF (Vascular Endothelial Growth Factor)
They are both Pro-angiogenic + vasodilatory

27
Q

Receptor that binds PLGF/VEGF

A

Flt1
soluble receptor binds soluble angiogenic factors to limit their bioavailability

28
Q

How does PE affect the action of PLGF/VEGF

A

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
Q

What are extracellular vesicles

A

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
Q

Role of extracellular vesicles

A

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
Q

Preeclampsia impact on extracellular vesicles

A

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
Q

Proposed mechanism behind PE

A

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
Q

What is the cause of later onset pre-eclampsia?

A

Not understood yet
suggested theory: women with genetic CVD risk manifest symptoms bc of pregnancy stress

34
Q

Timeline of PE development

A

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
Q

What is the consequence of placental ischaemia?

A

Fetal Growth Restriction (same as intra-uterine GR)

36
Q

What are the two stages of pre-eclampsia development?

A

Stage 1 (Abnormal Placentation) // Stage 2 (Maternal Syndrome)

37
Q

What are the factors that lead to stage 1?

A

Genetic (increased sFlt1 genes) // Environment (ckd, t2dm, htn) // Immunological

38
Q

What is the consequence of systemic vascular dysfunction in pre-eclampsia?

A

Proteinuria, Hypertension, Headache/Visual Disturbances , HELLP Syndrome, Eclampsia

39
Q

What are the two measurements that can be used to detect pre-eclampsia?

A

PLGF Levels (<100 is abnormal), high sensitivity and red diagnosis time
sFlt-1 : PLGF ratio (>38 is abnormal)

40
Q

Issues with PLGF/ sFlt1:PLGF

A

Not definitive
Cannot predict PE b4 onset. only useful post 20wks

41
Q

Future PE diagnosis methods

A

Examine cfRNA (cell free) from maternal blood
Examine small molecule metabolites in urine to reveal biosignatures

42
Q

What is SGA?

A

Small for Gestational Age - baby is < 10th centile

43
Q

What is severe SGA?

A

Baby is < 3rd centile

44
Q

What are the three subclassifications of SGA?

A

Small throughout pregnancy but healthy
Early growth is normal, slows later in pregnancy (IUGR/FGR)
Non-placental growth restriction (genes, metabolism, infection)

45
Q

What is the difference between SGA and IUGR?

A

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
Q

What are the two types of IUGR?

A

Symmetric, Asymmetric

47
Q

What are the difference in growth reduction patterns between asymmetric/symmetric IUGR?

A

Symmetric has a proportional reduction in growth Asymmetric is head&brain sparing - normal head shape but smaller abdomen and torso

48
Q

What is the relative difference in cell number and cell size between the the two types of IUGR?

A

Symmetric - Low cell number normal size
Asymmetric - Normal number low cell size

49
Q

Which of the two have a poorer prognosis?
Symmetric vs Asymmetric IUGR

A

Symmetric IGUR
also the rarer form

50
Q

Aetiology of asymmetric IUGR

A

Utero-placental insufficiency
Placenta cannot provide sufficient nutrients and development favours the brain
More pronounced features of malnutrition

51
Q

Aetiology of symmetric IUGR

A

Genetic disorder
Infection

52
Q

What 3 systems are implicated by IUGR

A

Cardio, Resp, Neuro

53
Q

How does IUGR affect the cardio system

A

cardiac hypertrophy, vasoconstriction -> remodelling of fetal vessels

54
Q

How does IUGR affect the Resp system

A

bronchopulmonary dysplasia, immature lungs

55
Q

How does IUGR affect the Neuro system

A

motor defects, cognitive impairments

56
Q

What are the two mechanisms of IUGR?

A

Villous Maldevelopment, (genetics)
Vascular Malperfusion (defect with EVT invasion)

57
Q

What is villous maldevelopment?

A

Villi do not form properly - impaired blood exchange - fetal impoverishment

58
Q

What is vascular malperfusion?

A

placental bed pathology -> blood supply does not perfuse through the placenta as it should

59
Q

What other condition is caused by vascular malperfusion?

A

Early Onset Pre-Eclampsia

Dev/Age (4 decks)

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