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Amars Semester Two cards > Repro 8 > Flashcards

Repro 8 Flashcards

1
Q

By roughly what day has the blastocyst fully embedded into the endometrium? Which two structures interact for implantation to occur?

A

By roughly day 10, the blastocyst has implanted into the endometrium.
The synctiotrophoblast interacts with the simple columnar epithelium of the endometrium.

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2
Q

Explain what is meant by the term ‘haemomonochorial’ when applied to the placenta

A

Only a single layer of trophoblast separates the foetal blood and maternal blood.

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3
Q

Describe the differences between primary, secondary and tertiary villi, when discussing implantation.

A

Primary

  • day 13
  • finger like projections of trophoblast

Secondary

  • day 15-16
  • invasion of mesenchyme into the core

Tertiary

  • day 23
  • invasion of foetal blood vessels into mesenchyme
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4
Q

Name two implantation defects and briefly describe them and their associated risks.

A
  1. Ectopic pregnancy
    - implantation at a site that is not the uterine body
    • commonly the Fallopian tubes
    • can be ovarian or peritoneal
      - can become life threatening very quickly
  2. Placenta praevia
    - implantation in the lower uterine segment
    - can cause haemorrhage in pregnancy
    - requires C-section delivery
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5
Q

What is decidualisation?

A

This provides a balancing force for the invasive force of the trophoblast. It ensures the trophoblast doesn’t invade further than it needs to.

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6
Q

Why do you think there is a risk of haemorrhage in ectopic pregnancy?

A

The decidual cells are present in the uterus so they can control implantation invasive force.
In sites that are not the uterus, there are no decidual cells so there is no balancing force in terms of invasive force. Therefore there is nothing to stop the trophoblast from invading further and further. There are many arteries nearby so they can easily become invaded

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7
Q

What does remodelling of the spiral arteries achieve ?

A

Creates a low resistance vascular bed which can maintain the high flow required to meet foetal demand.
Very important in late gestation.

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8
Q

What is pre eclampsia and how is it characterised?

A

It is a pre cursor to maternal seizures (eclampsia)

Characterised by proteinuria and hypertension.

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9
Q

Describe the features of first trimester placenta

A
  • Relatively thick, so it acts as a barrier to diffusion

- cytotrophoblast layer beneath the synctiotrophoblast

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10
Q

Describe the features of a term placenta

A
  • Very thin - allows diffusion to take place easily
  • no cytotrophoblast beneath the synctiotrophoblast
  • surface area available for diffusion increased massively.
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11
Q

What are cotyledons and how are they formed ?

A

Decidual septum forms and projects into the intervillous space of the placenta. It doesn’t reach the chorionic plate but it divides the placenta. These divisions are called cotyledons.

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12
Q

The placental barrier gets thicker as pregnancy proceeds, to ensure the foetus gets blood supply constantly as its metabolic demands increase, particularly due to the brain getting larger. True or false?

A

False.
The placental barrier gets smaller as pregnancy proceeds.
At week 38, it’s roughly 5 micrometers compared to 40 micrometers at week 14.

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13
Q

Describe the arrangement of foetal blood vessels within the placenta.

A

Umbilical arteries and veins project into the tertiary villi, which are bathed in maternal blood.

2 Umbilical arteries carry DEOXYGENATED blood from the foetus back to the placenta.
1 umbilical vein carries OXYGENATED blood from the placental blood to the foetus.

Cotyledons receive blood from the spiral arteries, which are high pressured. This forces blood out of the arteries into the intervillous spaces.

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14
Q

Name some functions of the placenta

A

Metabolism
Transport
Endocrine

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15
Q

Describe the metabolic function of the placenta.

A

Synthesises:

  • glycogen
  • fatty acids
  • cholesterol
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16
Q

Outline the endocrine function of the placenta.

A

Secretes steroid and protein hormones.

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17
Q

What steroid hormones does the placenta secrete and what is the function?

A

These are released to maintain the pregnant state. They take over from the corpus luteum around week 11.

Progesterone and oestrogen are secreted
- progesterone increases appetite, which lays down fat stores for when the metabolic demands of the foetus increase in later pregnancy.

18
Q

What protein hormones are secrete from the placenta and what is their function?

A

hCG

  • secreted from the synctiotrophoblast in the first two months
  • supports the secretory function of the corpus luteum
  • absence of this hormone within the luteal phase leads to break down of the corpus luteum. It’s the signal it waits for.
  • pregnancy specific

Human chorionic somatomammotrophin (hCS)
- influences metabolism. It increases the amount of glucose available to the foetus. Achieved by causing insulin resistance.

hPL - insulin resistance

hCT and hCC

19
Q

What is the basis for pregnancy tests based on urine sample?

A

hCG is released from synctiotrophoblast and is therefore pregnancy specific.
It’s released in the urine so therefore testing the urine for the presence of this hormone is diagnostic.

20
Q

What is a ‘hydatidiform mole’

Name one other disease that falls under the same category of diseases

A

This is a trophoblast disease.
This is a molar pregnancy, where there is a ‘pregnancy’ without a conceptus. It’s essentially uncontrolled synctiotrophoblast.

Another disease is choriocarcinoma.

21
Q

Identify and outline the way major substances are transported across the placenta by simple diffusion

A
  • down concentration gradient
  • water
  • electrolytes
  • urea and uric acid
  • gases

GLUCOSE - facilitated diffusion not active transport or simple diffusion!

22
Q

Identify the major substances which are actively transported across the placenta

A
  • amino acids
  • iron
  • vitamins

Specific transporters are expressed by the synctiotrophoblast.

23
Q

Describe the placenta as a provider of passive immunity from the mother to the neonate

A

Foetus can make all of the components of complement by the end of the first trimester.
- week 14 - maternal IgG passes to foetus via receptor mediated pinocytosis.

24
Q

What are the signs in a foetus that rubella has crossed the placenta?

A

PDA
Cataracts
Microcephaly.

25
Q

Name 5 infectious agents that can cross the placenta

A 
Toxoplasma gondii
Rubella
Cytomegalovirus
Varicella zoster
Treponema pallidum
26
Q

Name some teratogens

A

Thalidomide
Alcohol
Pharmacological drugs

Drugs of abuse
Maternal smoking
(These two aren’t teratogenic)

27
Q

During the week of 2s, what cell layers emerge?

A

From the outer cell mass:
Synctiotrophoblast and cytotrophoblast

From the inner cell mass:
Epiblast and hypoblast

28
Q

Outline the maternal cardiovascular adaptations to pregnancy

A

Blood volume increases
Remember stroke volume x heart rate = cardiac output
All of these increase during pregnancy.
- changes on auscultation would also occur

29
Q

In a completely healthy pregnant lady, why would you expect to see changes in an ECG, which is perfectly normal?

A

There is an upward displacement of the diaphragm.

Therefore this causes some non pathological changes in the ECG.

30
Q

What causes systemic vascular resistance to decrease during T1?

A

Progesterone secretion.

31
Q

What changes would you expect to see in blood pressure of a pregnant lady and when would these normalise?

A

In T1-T2 expect to see a reduced blood pressure, which normalises during T3.
If see blood pressure raised, then this is a cause for concern.

32
Q

Outline the renal changes observed in pregnancy

A
  • Increase in GFR and renal plasma flow

- functional renal reserve decreases as the GFR increases

33
Q

What causes urinary stasis and what are the possible consequences of this?

A

Progesterone causes relaxation of the smooth muscle in the walls of the ureters. This causes stasis.

  • UTI
  • hydroureter
  • pyelonephritis (can induce pre term labour)
    • infection of the kidney, renal calyces.
34
Q

Why do the kidneys reabsorb less bicarbonate?

A

Progesterone drives hyperventilation so the mother can blow off extra co2 the foetus produces

  • this causes respiratory alkalosis
  • kidney compensates by reabsorbing less bicarbonate
35
Q

Outline some respiratory changes in pregnancy

A
  • A-P diameter of the thorax increases
  • alveolar ventilation rate increases
  • oxygen consumption increases
  • tidal volume increases
  • decreased functional residual capacity
  • respiratory rate is unchanged.
36
Q

What are the risks associated with poor control of gestational diabetes?

A

Macrosomic foetus
Still birth
Congenital defects risk increases

37
Q

Describe the changes seen in lipid metabolism during pregnancy

A
  • increase lipolysis from T2
  • increased fatty acids on fasting
    • leaves glucose for the foetus to use and the mother uses fatty acids as substrates for maternal metabolism
    • produces ketones
    • alkalosis and ketones is bad news.
38
Q

Give an example of anatomical changes in the GI system seen in pregnancy

A

Appendix can move from RLQ to RUQ

39
Q

Why do you think there is an increased risk of pancreatitis during pregnancy?

A
  • raised level of circulating fatty acids - Hyperlipidaemia

- formation of gall stones can lead to pancreatitis

40
Q

Why can warfarin not be given in pregnancy.

A

It crosses the placenta and is a teratogen.

41
Q

Describe why physiological anaemia occurs in pregnancy

A

Plasma volume increases but the RBC volume doesn’t increase to the same proportion - there is a mismatch which leads to physiological anaemia.

42
Q

Give some signs and symptoms of pre eclampsia.

A 
Proteinuria
Hypertension
Vasoconstriction
Plasma contracted
Pitting oedema.

Amars Semester Two cards (37 decks)

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