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Reproduction - Lian > Reproduction 8 - Pregnancy > Flashcards

Reproduction 8 - Pregnancy Flashcards

0
Q

What cells/layers are involved in implantation?

A

Interaction between Trophoblast cells and the epithelium of the uterus.

Further embedding of the blastocyst into the endometrium is dependent upon the invasive property of the trophoblast cells, which by now have an outer layer called the Syncitiotrophoblast differentiated from the underlying Cytotrophoblast.

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1
Q

Draw a diagram to show implantation of the blastocyst

A

see notes

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2
Q

Implantation is said to be interstitial. What does this mean?

A

Uterine epithelium is breached and conceptus implants within stroma

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3
Q

Outline 3 aims of implantation

A

1) Establish the basic unit of exchange (primary, secondary & tertiary villi)
2) Anchor the placenta (establishment outermost cytotrophoblast shell)
3) Establish maternal blood flow within the placenta

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4
Q

Draw a labelled diagram of villi

A

See notes

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5
Q

Draw/label a diagram of embryo & placenta.
Label: the Decidua basalis, decidua capsularis, Decidua parietalis, chorion frondsum, chorion laeve, amniotic cavity, chorionic cavity, yolk sac, uterine cavity

A

See notes

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6
Q

How does the endometrium prepare for implantation/ the placenta?

A
  • Decidualisation (stimulated by progesterone). The decidual reaction provides the balancing force for the invasive force of the

-Remodelling of Spiral Arteries; Creation of low resistance vascular bed
Maintains the high flow required to meet fetal demand, particularly late in gestation

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7
Q

Outline 3 implantation defects

A

1) ECTOPIC PREGNANCY
▪ Implantation at site other than uterine body
▪ Most commonly fallopian tube
▪ Can be peritoneal or ovarian
▪ Can very quickly become a life-threatening emergency

2) PLACENTA PRAEVIA
▪ Implantation in the lower uterine segment
▪ Can cause haemorrhage in pregnancy
▪ Requires C-Section delivery

3) INCOMPLETE INVASION
▪ Placental insufficiency
▪ Pre-eclampsia

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8
Q

What is the fetal portion of the placenta formed of and bordered by?

A

o Formed by the chorion frondsum

o Bordered by the chorionic plate

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9
Q

What marks the maternal portion of the placenta?

A

o Formed by the decidua basalis

o The decidual plate is most intimately incorporated into the placenta

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10
Q

What is between the chorionic and decidual plates?

A

Intervillous Spaces, which are filled with maternal blood.

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11
Q

Where are the decidual septa found and what do they do?

A

Project into the intervillous spaces of the placenta but do not reach the chorionic plate.

These septa divide the placenta into a number of compartments or Cotyledons.

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12
Q

What proportion of the uterus does the placenta cover?

A

15 – 30% of the internal surface

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13
Q

What is different about a term placenta?

A

o Surface area for exchange dramatically increased
o Placental ‘barrier’ is now thin
o Cytotrophoblast layer beneath syncytiotrophoblast lost

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14
Q

What do the umbilical veins & arteries project into?

A

Tertiary villi - bathed in oxygenated maternal blood.

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15
Q

Describe the fetal blood vessel arrangement in the placenta

A

Two Umbilical Arteries
o Deoxygenated blood Fetus –>Placenta

One Umbilical Vein
o Oxygenated blood Placenta –> Fetus

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16
Q

What factors influence passive diffusion across the placenta?

A

o Concentration Gradient
▪ The steeper the gradient, the more diffusion
o Barrier to diffusion
▪ Placental membrane gradually thins throughout pregnancy as the demand of the fetus increases
o Diffusion distance
▪ Haemomonochorial

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17
Q

Identify the major substances which are actively transported across placenta

A

Specific transporters are expressed by the syncytiotrophoblast
o Amino acids
o Iron
o Vitamins

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18
Q

What substances diffuse across the placenta?

A 
Simple Diffusion
o Water
o Electrolytes
o Urea and uric acid
o Gases
▪ Flow limited, not diffusion-limited
▪ Fetal O2 stores are small – maintenance of adequate flow is essential

Facilitated Diffusion
o Glucose

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19
Q

How is the placenta not a ‘true’ barrier?

A 
Teratogens can access the fetus via the placenta & particularly damaging during critical stages of development. For example -
o Thalidomide
o Alcohol
o Therapeutic drugs
o Drugs of abuse
o Maternal smoking
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20
Q

List 5 pathogens able to cross the placenta

A 
o Varicella zoster
o Cytomegalovirus
o Treponema Pallidum
o Toxoplasma gondii
o Rubella
21
Q

What two classes of hormones does the placenta produce - list them

A

1) Steroid: oestrogen & progesterone

2) Protein: 
Human Chorionic Gonadotrophin (hCG)
Human Chorionic Somatommotrophin (hCS)
Human Chorionic Thyrotrophin
Human Chorionic Cortiotrophin
22
Q

When is hCG produced and what does it do?

A

▪ Produced during the first two months of pregnancy & by the syncytiotrophoblast, therefore is pregnancy specific.

▪ Supports the secretory function of the corpus luteum

▪ Excreted in maternal urine, therefore is used as the basis for Pregnancy Testing

23
Q

Human Chorionic Somatommotrophin (hCS)

A

Influences maternal metabolism, increasing the availability of glucose to the fetus

24
Q

Other than hormones, what else does the placenta synthesise?

A

Glycogen, cholesterol and fatty acids.

25
Q

What is progesterone produced by and what is its impact on pregnancy

A

▪ Placenta takes over production from the corpus luteum (Week 11)
▪ Influences maternal metabolism by increasing appetite

26
Q

How does the placenta provide passive immunity?

A

Immunological competence begins to develop late in the first trimester, by which time the fetus makes all of the components of complement.

Fetal immunoglobulins consist almost entirely of Maternal Immunoglobulin (IgG), which begins to be transported from mother to fetus at approximately 14 weeks. The IgG is transported via Receptor Mediated Pinocytosis. Eventually the concentration of IgG in fetal plasma exceeds that of maternal plasma.

In this manner the fetus gaines passive immunity against various infectious diseases. Newborns produce their own IgG, but adult levels are not attained until the age of 3.

27
Q

What is Haemolytic Disease of the Newborn?

A

Rhesus alloimmunisation - Rhesus blood group incompatibility of mother and fetus
o Mother previously sensitised to rhesus antigen (e.g. previous pregnancy)
o IgG against rhesus crosses the placenta and attacked foetal RBCs
o Now uncommon because of prophylactic treatment
▪ Rhesus –‘ve mothers pregnant with Rhesus +’ve fetus given Rhesus specific IgG throughout pregnancy, to prevent sensitisation in the event of exposure to the antigen (The given IgG will bind to antigen before the mother’s immune system can mount a response)

28
Q

What is the effect of pregnancy on the cardiovascular system? Why does blood pressure not rise?

A 
o Blood volume increases
o Cardiac output increases
o Stroke volume increase
o Heart rate increases
o Systolic BP is never increased in Pregnancy (normally) - progesterone lowers vascular resistance
29
Q

How might hypotension in Pregnancy arise?

A

▪T1 and T2 – Progesterone effects on Systemic Vascular Resistance (SMV)
▪ T3 – Aortocaval compression by gravid uterus. Reduced return to the heart.

30
Q

Why can pregnant women get urinary stasis and what is this associated with?

A

Progesterone relaxes the smooth muscle in the walls of the ureters, which can result in stasis, hydroureter, UTIs and pyelonephritis.

Pyelonephritis can induce pre-term labour.

31
Q

In relation to the urinary system, what things increase during pregnancy?

A

o Renal plasma flow (RPF)
o Glomerular Filtration Rate (GFR)
o Creatinine clearance
o Protein excretion

32
Q

Consider the urinary system - what plasma metabolites decrease?

A

Urea, uric acid, bicarbonate & creatinine

33
Q

What is the physical impact of pregnancy in the respiratory structures?

A

o Diaphragm is displaced

o A-P and transverse diameters of thorax increase

34
Q

What drives physiological hyperventilation in pregnancy and what its significance?

A

Driven by progesterone, so the mother can blow off the extra CO2 the fetus produces.

35
Q

What does physiological hyperventilation lead to and how does the body compensate?

A

This leads to respiratory Alkalosis, which the kidneys compensate for by producing and reabsorbing less bicarbonate.

36
Q

How does carbohydrate and fatty acid metabolism vary over pregnancy?

A

Glucose and amino acid metabolism are altered in pregnancy to favour nutritional supply to the fetus. The fat which is laid down in the first half of pregnancy in the mother helps meet the demands of the fetus later in the pregnancy when the fetus is most demanding, metabolically.

Progesterone stimulates appetite in the first half of pregnancy and diverts glucose into fat synthesis. Oestrogen stimulates an increase in prolactin release, which, along with other hormones, generates a maternal resistance to insulin. Maternal glucose usage thus declines and gluconeogenesis increases, maximising availability of glucose to the fetus.

In later pregnancy, the mother’s energy needs are met by metabolising peripheral fatty acids.

37
Q

What hormone leads to increase in maternal insulin resistance?

A

Oestrogen stimulates an increase in prolactin release, which, along with other hormones, generates a maternal resistance to insulin.

38
Q

How would you test for gestational diabetes?

A

Oral glucose tolerance test

39
Q

What risks are associated with gestational diabetes?

A

▪ Macrosomic fetus
▪ Stillbirth
▪ Increased risk of congenital defects

40
Q

The rate of secretion of insulin (both basal and stimulated) normally increases as pregnancy proceeds. How does the pancreas meet this demand?

A

b-cell hyperplasia and hypertrophy as well as the increased rate of insulin synthesis in the b-cell.

41
Q

Outline changes in maternal lipid metabolism during pregnancy

A

o Increase in lipolysis from T2

o Increase in plasma concentration of free fatty acids on fasting
▪ Free fatty acids provide substrate for maternal metabolism, leaving glucose for the fetus

o Increased utilisation of free fatty acids increases the risk of Ketoacidosis

42
Q

Describe the changes in the maternal thyroid during pregnancy

A

o Thryoid binding globulin production increased
o T3 increased
o T4 increased

Free T4 in normal range due to increased binding globulin

43
Q

How does hCG effect the thyroid and why might TSH be lower in some normal pregnancies?

A

o hCG has a direct effect on the Thryoid, stimulating T3 and T4 production
▪ TSH can be decreased as a result of negative feedback from T3 and T4 produced due to hCG secretion

44
Q

Describe (with examples) the anatomical and physiological changes of the GI system during pregnancy

A

Anatomical Changes
o Alterations in the positions of viscera
▪ E.g. appendix moves from RLQ to LUQ as the uterus enlarges

Physiological Changes
o Smooth muscle relaxation by Progesterone
▪ GI – Delayed emptying
▪ Biliary tract – Stasis
▪ Pancrease – Increased risk of pancreatitis

45
Q

How does thromboembolic disease arise during pregnancy? And why can you not give warfarin to treat?

A

o High amount of fibrin deposition at the site of implantation
▪ Increased fibrinogen and clotting factors
▪ Reduced fibrinolysis - stasis, venodilation
▪ Cannot give warfarin – crosses the placenta and is teratogenic

46
Q

Discuss anaemia during pregnancy

A

o Plasma volume increases
o RBC mass also increases, but not to the same degree
o Physiological anaemia (Not a true anaemia, just a mismatch between volume and haemocrit)

o Anaemia due to iron and folate deficiency can also occur

47
Q

How might maternal Grave’s disease & Hashimoto’s thyroiditis effect the developing fetus?

A

Antibodies will cross the placenta and either stimulate TSH receptors on or destroy developing fetal thyroid respectively.

48
Q

Outline the aims of antenatal screening

A

▪ Risk factors – E.g. for gestational diabetes
o Blood test - Blood group, Haemoglobin, Infection
o Urinalysis - Protein
o Ultrasound - Estimation of fetal age, height/weight

49
Q

List the features of a pre-eclamptic pregnancy

A 
o Vasoconstricted
o Plasma-Contracted
o Raised blood pressure
o Proteinuria
o Pitting oedema

Reproduction - Lian (9 decks)

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