Session 8 - Group work Flashcards Preview

Semester 4 - Reproductive System > Session 8 - Group work > Flashcards

Flashcards in Session 8 - Group work Deck (37)
1

What effects would you expect maternal smoking to have upon the placenta? What
effect may this have upon the baby?

May reduce placental blood flow and growth. Poorer fetal nutrition will reduce birth weight,
by on average, 200g.

2

How does alcohol cross the placenta? What implications does this have for the
development of a baby whose mother drinks significantly during pregnancy?

By diffusion – lipid soluble
Possible cause of Fetal Alcohol Syndrome in which the maternal (mis)use of alcohol leads to
a fetus of low weight and with growth retarded (potentially with mental retardation, head and
facial abnormalities)

3

Why might cytomegalovirus, which normally just causes a mild flu-like illness in
infected adults, be a significant health hazard in pregnancy?

Can cause teratogenesis

4

1 Following the birth of a rhesus positive baby to a rhesus negative mother it is
customary to administer ‘anti-D therapy’ in the form of anti-D antibody. Why is this
done?

Mother may have made antibodies to fetal Rhesus antigens if fetal blood has entered the
maternal circulation. The anti-D antibody neutralises these antigens. The presence of
maternal anti-Rh antibodies in the fetal circulation causes rapid haemolysis when they bind
to the fetal red blood cells. (The Kleihauer test is used to demonstrate the presence or
absence of fetal cells in the mother's circulation (which is especially important in Rh
isoimmunization). If the foetal cells contain antigens which the mother's cells lack then the
mother could raise antibodies against these antigens.)

5

In the third stage of labour, what tissue of maternal genetic origin is shed with the
afterbirth?

The decidua

6

From where does the IgG in fetal blood derive?

the mothers blood

7

Could, in principle, a neonatal immune disease be mediated by IgM? If not, why not

No, because the IgM class of antibodies does not cross the placenta

8

i) hCG is released from trophoblastic cells (syncytiotrophoblasts) of the blastocyst
peaking at 10 weeks gestation

ii) hCG (human chorionic gonadotrophin) mimics the action of LH on the corpus
luteum, hence preventing degeneration of the latter

iii) Oestrogen and especially progesterone secretion is important in maintaining
pregnan

How does early pregnancy support itself?

hCG is released from cells of the developing fertilized ovum. By stimulating the corpus
luteum, hCG maintains (and indeed increases) the release of progesterone and oestrogen
characteristic of the luteal phase of the menstrual cycle. Hence, oestrogen and progesterone
maintains the endometrium and hence the pregnancy.

9

hCG reduces maternal IgA, lgG and 1gM. Speculate
(i) why may this benefit the fetal-placental unit?
(ii) what consequence may it have on the mother?

) Humeral immunity is depressed and is probably necessary to stop rejection of the
placenta by the mother and vice-versa.
ii) The mother is more susceptible to viral infections

10

Progesterone relaxes smooth muscle. Identify two effects increasing progesterone
levels may therefore have on GI tract function that the mother may complain of?

By reducing motility it may lead to heartburn and constipation.

11

Oestrogen and progesterone both stimulate breast growth, along with which other
hormone from the anterior pituitary?

Prolactin

12

Explain how inhibin (from the corpus luteum and placenta) prevents further
pregnancies occurring?

Suppresses FSH secretion, hence blocking follicular growth

13

In early pregnancy, progesterone stimulates appetite and promotes maternal
deposition of fat (on average 3 kg of fat are accumulated by the mother; i.e. 25% of
her weight gain). How is this beneficial to the mother in later pregnancy and after the
birth of the baby?

Maternal preparation e.g. breast growth, and also may provide a reserve for later pregnancy
when fetal demands are greater. In later pregnancy fat rather than glucose is the primary
source of energy for the mother.

14

4 The above process can lead to maternal hypoglycaemia between meals. However,
hPL (hCS) also promotes lipolysis. How is this of value?

Lipids and ketones released are available for energy. In early pregnancy, progesterone
increases maternal appetite and promotes the storage of glucose in fat stores. hPL (hCS)
promotes lipolysis of these fat stores.

15

Plasma volume increases by about 50%, (red cell mass by about 20%). Cardiac
output increases from 4.5 to 6 L/min. This is achieved mainly through increase in
stroke volume as compared to heart rate (18%). What change in mother’s blood
pressure do these adjustments induce? (TPR changes considered in question 8.25,
below)

Mean BP remains the same, but the increased stroke volume raises systolic BP a little and
the stroke volume, flowing so rapidly into additional tissue, reduces diastolic BP a bit.

16

Hence, what changes in the heart may be apparent on examination?

Upward displacement, hypertrophy, flow murmurs are common.

17

However, remembering that progesterone levels are continually increasing and also
considering its effect on smooth muscle, how may mean arterial blood pressure be
affected by progesterone? What may the mother notice due to those changes?

Peripheral vasodilation which may cause hypotension.(mean arterial blood pressure = total
peripheral resistance x cardiac output, vasodilation cases a fall in TPR)

Peripheral vasodilation may be experienced as
‘feeling the heat'
easy to sweat
nasal congestion

18

Late pregnancy is associated with venous distension and engorgement. What factors
contribute to it? (Hints: consider previous questions and position of IVC)

smooth muscle relaxation by progesterone.

Mechanical pressure from the uterus compressing the IVC may increase lower limb venous
pressure, but only when mother is recumbent.

(consider also raised circulating blood volume)

19

What are the two long-term sequelæ that are attributed to this period of venous
distension? (Hint: Consider the legs and lower GI tract)

Varicose veins and haemorrhoids

20

What anatomical /mechanical affect will the expanding uterus have on the maternal
respiratory system?

Diaphragm rises and intercostal angle widens, the uterus exerting a mechanical limitation to
inspiration

21

After the gravid uterus rises from the pelvis it rests upon the ureters compressing
them above the pelvic brim. What possible effects might this have?

Increased intraureteral tone, urethral dilatation, hydro-ureter, hydronephrosis. This may also
be caused by the smooth muscle relaxation effect of progesterone.

22

2 Pregnancy may be associated with an increase in urinary incontinence. Why do you
think this might occur?

Pressure on the bladder from enlarged uterus. Engagement of the fetal head towards the
end of pregnancy

23

Progesterone dilates smooth muscle in the nephrons of the kidneys (collecting duct)
and ureters. Why might this increase the likelihood of urinary tract infections?

Dilation slows the excretion of urine, making UTI’s more common

24

The placenta also contributes to the maternal synthesis of DHCC (1,25
dihyroxycholecalciferol P3 or calcitriol). How does this active form of vitamin D3
contribute to fetal growth?

It increases uptake of calcium from the maternal gut. The increased availability of calcium to
the fetus facilitates skeletal formation and growth, etc.
(Expectant mothers are encouraged to increase their dietary calcium by up to 70%. PTH
(parathyroid hormone) also rises in the third trimester, enhancing calcium mobilisation from
maternal bone and increasing availability to the fetus.)

25

Explain why blood pressure should not be measured with the expectant mother lying
down, particularly in late pregnancy?

The uterus can compress the inferior vena cava, reducing venous return and hence,
lowering blood pressure (supine hypotensive syndrome)

26

How will the following physiological parameters change during pregnancy?

Cardiac output

Heart rate:

O2 consumption

Tidal Volume

Cardiac output: Increases by 40%
Heart rate: Increases to 80-90 bts per minute
O2 consumption: Increases by 15%
Tidal Volume Increased by 40%

27

If this diabetes is not controlled, how will sustained hyperglycaemia effect fetal
glucose levels and what will be the consequences to the fetus?

Fetal hyperglycaemia also.
The fetus increases insulin secretion (but is not exposed to same levels of hPL as mother).
As there is increased glucose available, it is stored as fat (fetal macrosomia). In particular,
the fetal liver enlarges (due to glycogen storage).

28

How may such changes create problems?


(a) during childbirth?
Difficult delivery due to large size of fetus, birth trauma such as brachial plexus injury;
caesarean section may be required.

(a) in the neonate?

Once isolated from the maternal supply of glucose, the neonate may experience a reflex
hypoglycaemia due to its high circulating levels of insulin. The brain is particularly at risk of
damage from hypoglycaemia as it does not have glycogen storage.

29

What other complications, to the fetus, are also associated with poorly controlled
maternal diabetes?

prematurity
Impaired lung maturation
respiratory disorders of newborn
cardiac, neural tube defects and other congenital malformations, may occur if conception
occurs during a period of maternal hyperglycaemia
polycythemia etc.

30

The fetal-placental unit clearly needs iron, but: - i) Why does the mother herself need more iron?
ii) How else is iron turnover changed in pregnancy?

i) For the Hb in her expanded blood volume.
Ii) Menstrual losses have stopped.

31

What symptoms may mother experience and what treatment will help her?

May be asymptomatic or easy fatigability or breathlessness
Oral iron sulphate or gluconate

32

Predict the consequences of poor fetal-placental perfusion associated with anaemia
in pregnancy?

Fetal growth retardation.
Anaemic women have 3-5 times higher mortality rate in pregnancy than non-anaemic
women and a still birth rate up to 6 times higher.

33

The mother admits smoking continually during her pregnancy. How will these affect
O2 flow to the fetus and by what mechanism?

Carbon monoxide in maternal blood shifts her Hb-O2 curve to the left, so the
fetus suffers a reduced pO2 in extracting its O2 requirement, which may not be fulfil

34

What are the diagnostic criteria for pre-clampsia?

Hypertension and proteinuria

Oedema may or may not be present and therefore is not included in the diagnostic signs.

35

What signs and symptoms suggest that a mild pre-eclampsia is worsening in
severity?

Increasing diastolic BP Lack of fetal growth
Persistent and worsening albuminuria Oligohydramnios
Oliguria Pulmonary oedema
Thrombocytopenia Headache
Elevated liver enzymes Visual complaints

36

If this patient’s blood pressure were to rise and the patient to have an eclamptic fit,
what would you do?


Initial management of eclamptic fit is to maintain maternal airway, administer oxygen, place
her on left side (enhance uterine perfusion) and maintain her safety during the convulsion.
Magnesium is given by intravenous bolus then continuous infusion to relieve vasospasm and
stop the fitting. Sometimes thiopentone or diazepam are needed for recurrent fits. Blood
pressure control usually requires hydralazine. Once stable assess fetus and maintain
optimum fluid/oxygen/positioning. Delivery is the definitive treatment for eclampsia.
Caesarean delivery will often be required unless the cervix is extremely favourable.

37

What complications are associated with multiple pregnancies?

Increased incidence of pregnancy induced hypertension
anaemia
polyhydramnios
preterm labour
perinatal mortality
antepartum haemorrhage.