Lecture 13: Pathological Pregnancies Flashcards

1
Q

In a broad sense what are the changes that occur in pregnancy?

A
  • Changes occur to most body systems
  • Maternal CV
  • Heamotological system
  • Maternal immune system
  • Genital system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the heamotological changes for mum in pregnancy?

A
  • Increased blood volume
  • Plasma and blood volume increase at differing rates
    = Heamatocrit falls as plasma increases at a higher rate than cell mass.
  • Plasma increases around 1250mls by 30 weeks and thereafter remains stable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the cardiovascular changes of pregnancy?

A

Most important:

  • Increased CO
  • > ~10% inc. SV, 10-15% inc HR
  • 50% increase Blood volume

= Reduced peripheral vascular resistance (i.e pre-eclampsia = higher than normal PVR)

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

How can estrogen cause CV adaptations?

A

Potentially oestrogen

  • Can reduce vascular resistance mainly in reproductive tissues
  • Can alter the ratio of type 1 : 3 collagen in the vessel wall
  • High levels of estrogen are not reached until 9 weeks when fetal adrenals induce synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How can progesterone cause CV adaptations?

A
  • Progesterone may induce vascular relaxation in the uteroplacental circulation but DOES NOT appear to ahve a systemic effect
  • Progesterone is alos not markedly elevated until 10 weeks pregnant.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the role of angiotensin in CV adaptations?

A
  • ANG2 (vasocon) increases in pregnancy…
  • The uteroplacental unit produces a large amount of RAS

BUT the effects of ANG2 appear to be blunted in pregnancy - Potentially due to changes in receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the role of NO in CV adaptations of pregnancy?

A
  • No is produced by vascular endothelial cells by NO synthetase in response to shear stress of blood flowing over the vessel surface.
  • T1/2 of six seconds and causes art. wall relaxation and dilation
  • The activity of NO synthetase is some tissues is increased in pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is preeclampsia?

A

Pre-eclampsia is a multi system disorder unique to human pregnancy

Characterised by hypertension and involvement of one or more other organ systems and/or the fetus.

Raised BP commonly but not always first manifestation.

Proteinuria is commonly recognised additional feature after hypertension. but not considered mandatory to make clinical diagnosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the clinical profile of preeclampsia?

A
  • Hypertension arises 20+ weeks gestation \accompanied by one or more of:
  • Renal involvement
  • Disseminated intravascular coagulation
  • Severe epigastric and/or right upper quadrant pain
  • Neurological involvement headache, visual disturbances
  • Stroke
  • Pulmonary oedema
  • FGR/IUGR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is believed to trigger preeclampsia?

A

Preeclampsia is a failed maternal adaptation

  • Triggered by something from the placenta
  • An exaggerated inflam response leading to vascular dysfunction
  • Failure of the normal CV adaptations to pregnancy
  • Loss of the normal decrease in maternal peripheral vascular resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the subgroups of pre-eclampsia?

A

Early onset; 20-30 weeks at diagnosis
late onset; 34+ weeks

Distinction important - usually but NOt always late onset is less severe.

Probably different causes and potentially treatments may differ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the cure for pre-eclampsia?

A
  • Delivery of the fetus to prevent progression of maternal signs/symptoms
  • Hypertension can be managed pharmacologically
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does pre-eclampsia dispose the mother to?

A

Early CV mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some of the risk factors for pre-eclampsia that can be addressed prior to pregnancy?

A

Just generic CV risk factors

- Smoking, hypertension, obesity, dyslipidemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Define SGA:

A

Small for gestational age

  • Compared to averages usually <10 centile
  • Includes constitutionally small babies
  • Easy and consistent to measure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is FGR?

A

Fetal growth restriction

- A fetus that has not reached its growth potential

17
Q

Is it easy to detect IUGR and FGR in utero?

A

Yes.
- Abnormal doppler waveforms of the uterine and umbilical art.

Long term consequences for survivors

18
Q

What is the pathophysiology of SGA/IUGR/FGR?

A

Issues with the uteroplacental circulation

i. e untransformed spiral arteries
- > Inadequate depth of trophoblast invasion into the spiral arteries.

19
Q

Describe the FGR palcenta:

A
  • Smaller in volume
  • Thinner
  • Decreased umbilical blood flow
  • Inadequately developed vasculature
20
Q

Why is it amazing that the fetus is not immunologically rejected?

A
  • Half maternal, half paternal
  • Yet for 9 months fetal tissue of the placenta, placental membranes survive intimate contact with maternal immune system.
21
Q

What is unique about the decidua when it comes to immunity?

A

The decidua contains

  • Almost no B cells
  • 10% of the leucocytes are T cells in the decidua
  • 70% of the leucocytes in the decidua are uterine NK cells, these lack CD16 required to effect ADCC
22
Q

How does the immune profile change in pregnancy?

A
  • Lymphocyte counts do not alter greatly in pregnancy but there is beleve to be a bias in the type of T- helper CD cells and the cytokines they produce with a tilt in the balance toward Th2 cytokines
  • Th2 cytokines drive the immune system towards an antibody mediated reponse. (instead of Th1 cytotoxic, immune rejection)
23
Q

Can the immune diminution of maternal immune response in pregnancy be problematic?

A

Some infections if first encountered in pregnancy may be more severe

  • Listeriosis has increased incidence in pregnancy
  • Some infections such as leprosy tend to be more severe in later pregnancy