6.1 part 2 Maternal Adaptations to Pregnancy

Question 1

What are the main maternal CVS changes seen during pregnancy? (4)

Answer 1

• increase plasma volume, CO, SV and HR
• decrease serum albumin and colloid osmotic pressure
• increase in coagulation factors and fibrinogen
• compression of IVC by uterus

Question 2

What is pre-load and after-load and how are these affected during pregnancy?

In what instance may this not be the case?

Answer 2

Pre-load is the volume of blood returning to the heart through RA
After-load is the resistance to blood flow exiting the LV

In pregnancy pre-load increases as there is increased blood volume and after-load decreases due to decreased TPR

Sometimes in late pregnancy when women is lying down, uterus can compress vena cava, decreasing return to the heart (pre-load) and resulting in vasovagal syncope

Question 3

What are the changes in cardiac size/position during pregnancy?

Answer 3

The heart is enlarged by both chamber dilation and hypertrophy.

Upward displacement of the diaphragm by the enlarging uterus causes the heart to shift to the left and anteriorly.

Question 4

Give 3 maternal changesto the renal system during pregnancy?

Answer 4

1) Increase in renal blood flow
2) IncreaseGFR ➞ functional renal reserve decreases and serum creatinine decreases
3) filtration capacity intact

Question 5

List the specific changes tobladder and ureter during pregnancy?

Why can this cause problems and 3 consequences of this

Answer 5

Bladder capacity doubles and there is dilation of the ureters due to progesterone

Can cause urinary stasis which can lead to:

1) hydroureter
2) obstruction
3) predispose women to UTI, specificallypyelonephritis

As a result of pyelonephritis, contractions may be stimulate which can result inPre-term labour

Question 6

What is the main maternal changeseen in the liver during pregnancy?

Answer 6

changes in oxidative liver enzymes eg. cytochrome P450

Question 7

Give 4 maternal GI changes seen during pregnancy?

Answer 7

1) nausea and vomiting
2) delayed gastric emptying
3) prolonged small bowel transit time(SM relaxation by
4) gastrointestinal reflux

Question 8

What are the changes in BP (systolic and diastolic) during pregnancy? What condition can this lead to and why?

Answer 8

Systolic BP is NEVER increased in pregnancy (normally)

Women may experience hypotension:
T1 & T2 – progesterone effects on SVR
T3 – Aortocaval compression by gravid uterus

Question 9

What happens to the endothelium of BV’s and the plasma during pregnancy?

How do these changes differ in a a pre-eclamptic pregnancy, why may this occur and what 3 things may this result in?

Answer 9

Normal pregnancy = Vasodilation (due to decreased TPR) and plasma-expanded

Pre-eclamptic pregnancy:
Vasoconstricted + plasma-contracted due to increased vascular permiability (lots of fluid leakage) and dailure of spiral artery remodelling causes insufficient blood flow. These can lead to…

1) Defect in placentation
2) Poor uteroplacental circulation
3) Widespread endothelial dysfunction

Question 10

What are the anatomical chest wall changes that occur during pregnancy?

Why do these increase?

Answer 10

The subcostal angle, the anterior-posterior, transverse diameters and the chest wall circumference all INCREASE

These changes compensate for the 4-cm elevation of the diaphragm so that the total lung capacity is not significantly reduced

Question 11

What changes occur to the following and why?

functional residual capacity (FRC)
tidal volume(TV)
vital capacity andtotal lung capacity (TLC)
alveolar ventilation/minute
RR

Answer 11

FRC is decreased due to the elevation of the diaphragm

TV increases due to the increase in the AP and transverse diameter

Vital capacity and TLC are unchanged

Alveolar ventilation/minute is Increased

RR is unchanged

Question 12

Why does pregnancy result in overall respiratory alkalosis and how is the compensated?

What is the hormone responsible for these changes

Answer 12

Due to physiological hyperventilation:

Increased metabolic CO2 production ➞increasedrespiratory drive ➞respiratory alkalosis ➞ compensated by increased renalHCO3 excretion

All controlled by Progesterone

Question 13

How does maternal carbohydrate metabolism ensure that glucose is used for the foetus? (incl hormones - CHOP)

What risk does this pose to the mother?

Answer 13

Glucose is preferential to the foetus. In order to ensure glucose is used by foetus and not by mother there is an increase in maternal peripheral insulin resistance. This means the mother will switch to gluconeogenesis and use alternative fuels for herself (lipolysis in T2)

Hormones involved are➞ cortisol, HPL, oestrogen/progesterone, prolactin

Risk: mother can become keto acidotic because lipolysis results in FA production which are metabolised in the liver to produce ketone bodies (decrease pH)

Question 14

How do blood glucose levels vary in pregnancy?

Answer 14

• Decrease in fasting blood glucose

* Increase in post-prandial blood glucose

Question 15

Give 4 risk factors for gestational diabetes? (F-POP)

Answer 15

• pre-existing diabetes
• obesity (BMI > 30)
• family history
• previous GD
• ethnicity (asian/African)
• previous child with fatal macrosomia (weight <4.5kg)

Question 16

Give 3 risks to the foetus if GD is controlled poorly and why?

Answer 16

• Macrosomic fetus
• Stillbirth
• Increased rate of congenital defects

Question 17

Why does Macrosomia occur with uncontrolled GD?

Give 2 significant neonatal risks/consequences?

What tests would be done?

Answer 17

In GD, the large amounts of glucose in blood cross placenta to foetus. Foetus pancreas responds by producing large amounts of insulin. As insulin stimulates storage of glucose it causes increased growth of baby ➞ macrocosmic

Neonatal risks

1) shoulder dystocia, can get stuck during birth and lead to fractures ➞ damage to brachial plexus can result in Erb’s or Klumpke’s palsy
2) metabolic problems: hyperglycaemia, hyperkalemia, hyperbilirubinemia

Oral glucose tolerance test required

Question 18

What is the effect of pregnancy on thyroid metabolism?

Answer 18

Pestrogen increases production of thyroid binding globulin which increases amount of T3 and T4 overall.

BUT remember 99% of T3 and T4 are bound hence the free T4 remains in normal range

Question 19

What is Hyperemesis gravidarum?

Answer 19

A pregnancy complication caused by increase hCG concentrations

It is characterised by severe nausea, vomiting, weight loss, and dehydration.

Question 20

How can Hyperemesis gravidarum lead to biochemical hyperthyroidism?

Answer 20

Due to the increased concentration of hCG.

hCG has an α subunit very similar to TSH, hence hCG can mimic TSH causing increased thyroid hormones in pregnancy.

Note: because of increased T3 and T4 by hCG the overall TSH level will slightly drop (due to negative feedback)

Question 21

What are the anatomical changes that occur in pregnancy?

Answer 21

Alterations in the disposition of the viscera

e.g. Appendix moves to RUQ as uterus enlarges

Question 22

Describe the haematological state during pregnancy

Answer 22

• Pregnancy is a pro-thrombotic state
• increased fibrin deposition at the implantation site
• Increased fibrinogen and clotting factors
• Reduced fibrinolysis
• Stasis due to venodilation

Question 23

What do the Haematological changes in pregnancy increase the risk of?

How would you treat?

Answer 23

Thromboembolic disease (increased risk of clotting -DVT)

Treatment: LMWH (low molecular weight heparin). Do NOT use Warfarin, as this crosses the placenta and is teratogenic

Question 24

List 4 clinical presentation signs of a PE in pregnancy

Answer 24

1) dyspnoea
2) palpitations
3) pleuritic chest pain
4) hemopytisis
5) tachycardia
6) cyanosis

Question 25

List 4 clinical presentation signs of a DVT in pregnancy

Answer 25

1) DVT usually proximal
2) unilateral pain/tenderness
3) swelling in extremity
4) increase in calf/thigh circumference
5) pitting oedema
6) increased temperature

Question 26

Why can anaemia occur in pregnancy?

Answer 26

This is physiological and due to the increase in plasma volume in disproportion to the RBCs. Red cell mass does increases, but less so ➞ dilution effect

Question 27

Why MUST early screening for haemoglobinopathies be done for couples during pregnancy?

Answer 27

To identify whether women or partner may be carriers as both thalassemia and sickle cell are autosomal recessive. If this is the case the couple is offered amniocentesis to check the foetal DNA and then discuss options

Question 28

sickle cell ➞ CPS ETA 1 revision

SCA is an autosomal _______ condition. SC trait is expressed as _______ and SC disease is _______.

It is caused by a base pair mutation of _______ to _______ resulting in an amino acid change from _______ to _______.

This results in a slightly reduced _______ charge which causes the RBC’s to become sickled in the _______ state (polymerised Hb). Repeated oxygenation/deoxygenation eventually causes cells to stiffen and remain distorted.

The 2 main consequences of this are _______ due to a shortened RBC lifespan and _______ due to RBC stiffness blocking capillaries.

Answer 28

recessive, HbAS, HbSS, adenine, thymine, glutamate, valine, negative, T, Hemolysis, Vaso-occlusion

Question 29

What is meant by “the foetus is an allograft”?

Describe the immune response and list 2 potential diseases that may cause problems with this

Answer 29

The foetus grows inside the mother and the mother accepts it and does not reject it as an organ. This requires non-specific suppression of the local immune response at the materno-foetal interface

The transfer of antibodies is usually beneficial however in the following cases it may cause problem:

• Haemolytic disease-e.g Rhesus incompatibility
• Graves disease and Hashimoto’s thyroiditis

Question 30

How can Graves disease in the mother cause problems to the foetus?

Answer 30

If a women has Graves, her IgG TSH antibodies will pass through the placenta into the baby. This can cause:

1) congenital heart block of the foetus
2) stimulate the foetal thyroid gland over-produce thyroid hormones ➞ neonatal thyrotoxicosis

Question 31

How can Congenital hypothyroidism develop in pregnancy and what are the consequences of this?

Answer 31

Congenital hypothyroidism is seen due to a deficiency in thyroid hormone of the mother.

Low T3 and T4 in the mother means there will be low levels of these crossing the placenta into the baby.

Baby is dependant on maternal thyroxine, hence if left untreated will lead to congenital hypothyroidism, handicap and in severe cases cretinism

Question 32

Describe how rhesus blood status can affect pregnancy for mother and foetus.

List two characteristics signs of a baby that has been affected by rhesus disease

Answer 32

If first baby is rhesus + and mother is rhesus -, then mother will develop antibodies against babies rhesus +. In first pregnancy this will not cause problem because antibodies take a while to develop.

However, in second pregnancy, the preformed antibodies will attack RBC’s of second foetus if that too is rhesus +. RBC’s will break down and release haemoglobin, this will be converted into bilirubin.

When baby is born they will be very jaundiced and anaemic