Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 1b - Development & Ageing > Disorders of Pregnancy & Parturition > Flashcards

Disorders of Pregnancy & Parturition Flashcards

1
Q

What is the importance of the placenta?

A

1st trimester:
* Embryo-fetal growth during the first trimester is relatively limited
* Low fetal demand on the placenta
* Early embryro nutrition is histiotrophic
* Reliant on uterine gland secretions and breakdown of endometrial tissues

2nd trimester:
* Fetal demands on placenta increase with pregnancy
* Switch to haemotrophic support
* Achieved in humans through a haemochorial-type placenta where maternal blood directly contacts the fetal membranes (chorionic villi)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When does foetal growth change from histitrophic to haemotrophic?

A
  • At the beginning of the 2nd trimester
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What allows the maternal blood to directly contact the fetal membranes in the placenta?

A
  • Chorionic villi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the structure of chorionic villi.

A
  • Finger-like extensions of the chorionic cytotrophoblast, which then undergo branching
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the function of the chorionic villi?

A
  • Provide substantial surface area for gas and nutrient exchange in the placenta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 3 phases of chorionic villi development?

A
  • Primary: outgrowth of the cytotrophoblast and branching of these extensions
  • Secondary: growth of the fetal mesoderm into the primary villi
  • Tertiary: growth of the umbilical artery and umbilical vein into the villus mesoderm, providing vasculature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens at the primary phase of chorionic villi development?

A
  • Outgrowth of the cytotrophoblast and branching of these extensions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens at the tertiary phase of chorionic villi development?

A
  • Growth of the umbilical artery and umbilical vein into the villus mesoderm, providing vasculature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens at the secondary phase of chorionic villi development?

A
  • Growth of the fetal mesoderm into the primary villi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are terminal villi?

A
  • Terminal villi are a specialized type of chorionic villus that are found at the ends of the branching chorionic villi
  • They are the site of the most active nutrient and gas exchange between the mother and fetus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How are terminal villi specialised for their function (2)?

A
  • Convoluted knot of vessels and vessel dilation
    • Slows blood flow enabling exchange between maternal and fetal blood
  • Whole structure coated with trophoblast (missing here as capillary cast)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do terminal villus change through the pregnancy?

A

Their diameter and the distance between the terminal villi and the maternal blood decreases.
* Early pregnancy: 150-200µm diameter, approx. 10µm trophoblast thickness between capillaries and maternal blood.
* Late pregnancy: villi thin to 40µm, vessels move within villi to leave only 1-2µm trophoblast separation from maternal blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are spiral arteries?

A
  • Spiral arteries provide the maternal blood supply to the endometrium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the purpose of spiral artery re-modelling?

A
  • Turns the spiral artery into a low pressure, high capacity conduit for maternal blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Outline the process of spiral artery remodelling (5 steps).

A
  1. Extra-villus trophoblast (EVT) cells coating the villi invade down into the maternal spiral arteries, forming endovascular EVT
  2. Endothelium and smooth muscle is broken down – EVT coats inside of vessels
  3. EVT cell invasion triggers endothelial cells to release chemokines, recruiting immune cells
  4. Immune cells invade spiral artery walls and begin to disrupt vessel walls
  5. EVT cells secrete break down normal vessel wall extracellular matrix and replace with a new matrix knowm as fibrinoid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What cells initiate spiral artery remodelling?

A
  • Extra-villus trophoblast (EVT) cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does a failed spiral artery remodelling look like on the cellular level (3)?

A
  • Smooth muscle remains
  • Immune cells become embedded in vessel wall
  • Vessels occluded by RBCs
18
Q

What are the consequences of a failed spiral artery remodelling?

A
  • Unconverted spiral arteries are vulnerable to pathological change including intimal hyperplasia and atherosis
    • This can lead to perturbed flow and local hypoxia, free radical damage and inefficient delivery of substrates into the intervillous space
  • Retained smooth musclemay allow residual contractile capacity -> perturb blood delivery to the intravillous space

Atherosis can also occur in basal (non-spiral) arteries that would not normally be targeted by trophoblast

19
Q

Outline the epidemiology of pre-eclampsia (PE).

A
  • Occurs in around 2-4% of pregnancies in USA and Europe
  • More common in Africa and Asia (8% to as high as 16%)
  • ~1/10 maternal deaths in Africa and up to 1/4 in South America are associated with gestational hypertensive disorders (including PE)
  • Estimated to cause 50,000-60,000 maternal deaths per year
Johnson et al – Essential Reproduction 7th Ed

Precise underlying causes remain a mystery

20
Q

What are the risk factors of pre-eclampsia (PE) (7)?

A
  • Previous pregnancy with pre-eclampsia
  • BMI > 30 (esp >35)
  • Fx
  • Increased maternal age (> 40) and possibly low maternal age (< 20)
  • Gestational hypertension or previous hypertension
  • Pre-existing conditions:
    • Diabetes
    • PCOS
    • Renal disease
    • Subfertility
    • Autoimmune disease (anti-phospholipid antibodies)
  • IVF pregnancy
21
Q

What are the 2 subtypes of pre-eclampsia (PE)?

A

Early onset: < 34 weeks
* Associated with fetal and maternal symptoms
* Changes in placental structure
* Reduced placental perfusion

Late onset: > 34 weeks
* More common (80-90% cases)
* Mostly maternal symptoms
* Fetus generally OK
* Less overt/no placental changes

22
Q

What role do placental defects play in pre-eclampsia (PE) pathogenesis?

A

Placental physiology:
1. Extra-villus trophoblast (EVT) invasion of maternal spiral arteries through decidua and into myometrium
1. EVT become endothelial EVT
1. Spiral arteries become high capacity

Vs

Pre-eclampsia placental pathogenesis:
1. EVT invasion of maternal spiral arteries is limited to decidual layer
1. Spiral arteries are not extensively remodelled
1. Placental perfusion is restricted

23
Q

What role do Flt1 and PLGF play in pre-eclampsia (PE) pathogenesis?

A

Placental physiology:
1. Releases PLGF and VEGF into the maternal circulation
1. These growth factors bind receptors on the endothelial surface to promote vasodilation, anti-coagulation and ‘healthy’ maternal endothelial cells

Vs

Pre-eclampsia placental pathogenesis:
1. Releases sFLT1, which acts as a sponge – mopping up PLGF and VEGF and stopping them binding to the endothelial surface receptors
2. In the absence of these signals, the endothelial cells become dysfunctional

24
Q

What is PLGF?

A
  • Placental Growth Factor (PLGF): VEGF related, pro-angiogenic factor released in large amounts by the placenta
25
Q

What is Flt1?

A
  • Flt1 (soluble VEGFR1): Soluble receptor for VEGF-like factors which binds soluble angiogenic factors to limit their bioavailabliltiy
26
Q

What causes later onset PE?

A

The underlying mechanisms are poorly understood:
* Current theory: maternal genetic pre-disposition to cardiovascular disease, which manifests during the ‘stress-test’ of pregnancy

27
Q

Outline the pathophysiology of pre-eclampsia (PE) (risks to mother 4 / risks to foetus 3).

A

Risks to Mother:
* Damage to kidneys, liver, brain and other organ systems
* Possible progression to eclampsia (seizures, loss of consciousness)
* HELLP syndrome: Hemolysis, Elevated Liver Enzymes, Low Platelets
* Placental abruption (separation of the placenta from the endometrium)

Risks to Fetus:
* Pre-term delivery
* Reduced fetal growth (IUGR/FGR)
* Fetal death (500,000/year worldwide)

28
Q

What is HELLP syndrome (3)?

A
  • Hemolysis
  • Elevated Liver Enzymes
  • Low Platelets
29
Q

How would a patient with pre-eclampsia (PE) present (6)?

A
  • New onset hypertension (in a previously normotensive woman) BP ≥140 mmHg systolic and / or ≥90 mmHg diastolic
    • Occurring after 20 weeks gestation
  • Reduced fetal movement and / or amniotic fluid volume (by ultrasound) in 30% cases
  • Oedema common but not discriminatory for PE
  • Headache (in around 40% of severe PE patients)
  • Abdominal pain (in around 15% of severe PE patients)
  • Visual disturbances, seizures and breathlessness associated with severe PE and risk of eclampsia (seizures)
30
Q

What investigations are recommended in a patient suspected with pre-eclampsia (PE) (2)?

A
  • PLGR levels
    • Rules out PE in next 14 days in women 20-36wks and 6d
  • sFlt-1/PlGF ratio
31
Q

What is the management of pre-eclampsia (PE) in < 34 week pregnancy (4)?

A
  • If < 34 weeks, preferable to try and maintain the pregnancy if possible for benefit of the fetus
    • Regular monitoring
    • Anti-hypertensive therapies
    • Magnesium sulphate to counter-act seizures
    • Corticosteroids for < 34 weeks to promote fetal lung development before delivery
32
Q

What is the management of pre-eclampsia (PE) in > 37 week pregnancy (1)?

A

Delivery preferable
* PE can only be resolved by delivery of the placenta

33
Q

What preventative therapies can be used in high risk pregnancies (3)?

A
  • Reduce BMI (esp if BMI >35)
  • Exercise throughout pregnancy (seems to work independent of BMI)
  • Low-dose asprin (from 11-14 weeks) for high risk groups – but may only prevent early onset
34
Q

What are the long-term health risks to a mother after pre-eclampsia (PE) (4)?

A
  • Elevated risk of cardiovascular disease
  • Type 2 diabetes
  • Renal disease
  • Roughly 1/8 risk of having pre-eclampsia in next pregnancy (greater if early onset)
35
Q

What foetal weight is classified as small for gestational age (SGA)?

A
  • < 10th centile (or 2 SD below pop norm)
36
Q

What foetal weight is classified as severe small for gestational age (SGA)?

A
  • 3rd centile or less
37
Q

What are the 3 subclassifications of small for gestational age (SGA)?

A
  • Small throughout pregnancy, but otherwise healthy
  • Early growth normal but slows later in pregnancy (FGR / IUGR)
  • Non-placental growth restriction (genetic, metabolic, infection)
38
Q

Define Interuterine Growth Restriction (IUGR) / Fetal Growth Restriction (FGR).

A
  • Interuterine Growth Restriction (IUGR) / Fetal Growth Restriction (FGR): fetuses / neonates with clinical features of malnutrition and in-utero growth restriction, irrespective of weight percentile
39
Q

What are the differences between symmetric and asymmetric Interuterine Growth Restriction (IUGR) / Fetal Growth Restriction (FGR)?

A
40
Q

Outline the pathogenesis of Growth Restriction (IUGR) / Fetal Growth Restriction (FGR).

A

Relatively unkown.

PE and FGR/IUGR – common causes?
41
Q

What are the pathophysiological complications of Interuterine Growth Restriction (IUGR) / Fetal Growth Restriction (FGR) to the foetus (Cardiovascular 2 / Respiratory 2 / Neurological 2)?

A

Cardiovascular:
* Foetal cardiac hypertrophy
* Re-modelling of foetal vessels due to chronic vasoconstriction

Respiratory:
* Poor maturation of lungs during foetal life, leading to bronchopulmonary dysplasia and respiratory compromise

Neurological:
* Long term motor defects
* Cognitive impairments

Phase 1b - Development & Ageing (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions