Session 8 - Pregnancy Flashcards

1
Q
A
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2
Q

Onw what day does the blastocyst implant into the endometrium?

A

6

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3
Q

What are primary, secondary, and tertiary placental villi?

A

Primary villi – early finger like projections into trophoblast
Secondary villi – invasion of mesenchyme into core
Tertiary villi – invasion of mesenchyme core by fetal vessels

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4
Q

What are the 3 pruposes of establishing a placenta

A
  • Anchor the placenta – via establishment of the outermost cytotrophoblast shell
  • Establish maternal blood flow within placenta
  • Establish basic unit of exchange ie villi
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5
Q

What is an ectopic pregnancy? What are the consequences?

A
  • Implantation at site other than uterine body, commonly fallopian tube
  • Can be peritoneal or ovarian
  • Can rupture and cause severe haemorrhage
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6
Q

What is placenta praevia? What are the consequences and how do you treat?

A
  • Placenta grows below os of uterus
  • Can cause haemorrhage in pregnancy
  • Requires C-section delivery
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7
Q
A
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8
Q

What is placental insufficiency?

A

insufficient blood flow to placenta during pregnancy caused by incomplete invasion of placenta

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9
Q

What is pre-eclampsia?

A

hypertension and large amount of protein in urine during pregnancy caused by incomplete invasion of placenta

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10
Q

How is the endometrium prepared for implantaiton?

A

Decidualisation – provides the balancing force for the invasive force of the trophoblast:

  • Stimulated by progesterone
  • W/o this complications such as haemorrhage can occur

Remodelling of spiral arteries:

  • Creates low resistance vascular bed
  • This maintains a high flow rate required to meet fetal demand.
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11
Q

What is the fetal portion and the maternal portion of the placenta made of?

A

Fetal - Formed by chorion frondsum

Maternal - Formed by decidua basalis

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12
Q
A
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13
Q

What is found between the chorionic and decidual plates of the placenta?

A

intervillous spaces which are filled with maternal blood

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14
Q

What are cotyledons of the placenta?

A

Decidual septa formed in the decidual plate divide the placenta into compartments or cotyledons

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15
Q

How does the thickness of the placenta change in the first and second trimester?

A

First trimester placenta:

  • Placenta established
  • Placental barrer to diffusion still thick
  • Complete cytotrophoblast layer beneath syncytotrophoblast

Second trimester placenta:

  • Loss of cytotrophoblast layer
  • Barrier thin
  • SA for exchange increased
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16
Q

Where do cotyledons recieve their blood from?

A

through spiral arteries that pierce the decidual plate.

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17
Q

Which substances are actively transported across the placenta? What about facilitated diffusion?

A

Active transport:

  • Amino acids
  • Iron
  • Vitamins

Facilitated diffusion:

  • Glucose
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18
Q

Give 3 examples of teratogens

A

thalidomide, alcohol, smoking

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19
Q

Give 2 examples of pathogens able to cross the placenta

A

Cytomegalovirus

Rubella

20
Q

Name the 4 protein and 2 steroid hormones produced by the placenta

A

Protein

  • hCG
  • hCS
  • hCT
  • hCC

Steroid:

  • Progesterone
  • Oestrogen
21
Q

How long is hCG produced for? What does it do?

A
  • produced during first 2 months of pregnancy
  • supports secretory function of corpus luteum
22
Q

What is the function of hCS?

A

influences maternal metabolism, increasing availability of glucose to fetus

23
Q

What does progesterone do during pregnancy?

A

influences maternal metabolism by increasing appetite

24
Q

What is the hormonal basis of testing for pregnancy?

A

hCG pregnancy specific and excreted in maternal urine

25
Q

How does the placenta provide passive maternal immunity to the neonate?

A
  • fetal immunoglobins consist of maternal IgG which are transported from mother at approx. 14 weeks
  • IgG transported via receptor mediated pinocytosis
26
Q

What is haemolytic disease of the newborn? How is it treated?

A
  • IgG antibodies produced by mother attacks RBCs of neonate.
  • Due to incompatability of rhesus blood groups between mother and fetus.
  • Mother prevbiously sensitised to rhesus antigen e.g. prevbious pregnancy
  • Treated with prophylactic treatment
27
Q

What happens to CO, BV, SV, HR, BP during pregnancy?

A

all but BP increaeses. BP decreases.

28
Q

Why is there a decrease in BP during pregnancy?

A
  • T1 and T2 – progesterone effects on systemic vascular resistance
  • T3 – aortocaval compression by gravid uterus results in reduced return to heart. Can result in syncope when lying in supine position. Roll woman on left to relieve compression.
29
Q

What happens to renal plasma flow, GFR, Creatinine clearance, protein excretion, plasma urea, plasma uric acid, plasma bicarbonate during pregnancy?

A

Plasma urea, uric acid, and bicarbonate decrease

Rest increases

30
Q

Why can urinary stasis occur during pregnancy? What are the possible consequences of this?

A

Progesterone relaxes smooth muscle of ureter which can result in stasis, hydroureter, UTIs, and pyelonephritis (PN can induce pre-term labour)

31
Q

Why does the mother go into physiological hyperventilation? How does this occur? What happens to plasma pH and how do the kidneys compensate?

A
  • Pregnancy results in physiological hyperventilation driven by progesterone so mother can blow off extra CO2 produced by fetus:
  • Leads to resp alkalosis, which kidneys compensate for by producing and reabsorbing less bicarbonate
32
Q

How does the metabolism of carbohydrates change for the mother? How do the hormones help do this?

A
  • Progesterone stimulates appetite in first half of pregnancy and diverts glucose into fat synthesis
  • Oestrogen stimulates increase in prolactin release, generates maternal resistance to insulin
  • Maternal glucose usage thus declines and gluconeogenesis increases, maximising availability of glucose to fetus
  • Later in pregnancy, mother’s energy needs are met by metabolising peripheral fatty acids
33
Q

What is gestational diabetes? What are the risks associated with it?

A

Carb intolerance first recognised in pregnancy and does not persist after delivery

Risks associated with poor control:

  • Macrosomic getus
  • Stillbirth
  • Increased risk of congenital defects
34
Q

How does the insulin production change as pregnancy proceeds? Why do some women develop gestational diabetes as a result?

A
  • Rate of secretion of insulin increases as pregnancy proceeds
  • Achieved by beta cell hyperplasia and hypertrophy and increased rate of insulin synthesis in beta cell
  • In some women, endocrine pancreas unable to respond to metabolic demand of pregnancy and cannot release enough insulin, results in loss of control of metabolism, blood glucose increases and diabetes results
35
Q

How does plasma conc of FFAs change during pregnancy and why?

A

Increase in plasma conc of FFAs during fasting for mother to use, sparing glucose for fetus

36
Q

How does levels of T3 and T4 change and why?

A
  • Thyroid binding globuilin production increased
  • Therefore T3 and T4 increased
  • BUT free T4 still in normal range
37
Q

How does the smooth muscle relaxation of the GI system impact it?

A
  • Delayed emptying of GI
  • Biliary tract stasis
  • Increased risk of pancreatitis
38
Q

Why does a physiological anaemia develop during pregnancy?

A
  • Plasma volume increases
  • RBC mass also increases
  • Physiological anaemia results – due to mismatch between volume and haemocrit
39
Q

What is an allograft?

A

Genetically different, same species

40
Q

What are the hallmark features of pre-eclampsia and how does this compare to a normal pregnancy?

A

Normal pregnancy:

  • Vasodilated
  • Plasma expanded

Pre-eclamptic pregnancy:

  • Vasoconstricted
  • Plasma contracted
  • Raised blood pressure
  • Proteinuria
  • Pitting oedema
41
Q

What hormone can be used to measure fetal progress?

A

estriol. Low levels can indicate fetal distress

42
Q

How much is cardiac output increased by in pregnant women?

A

40%

43
Q

How much is HR increased by in pregnant women?

A

to 80/90

44
Q

How much is o2 consumption increased by in pregnant women?

A

15%

45
Q

How much is tidal volume increased by in pregnant women?

A

40%

46
Q

What is reflex hypoglycaemia in a child?

A

If uncontrolled maternal diabetes occurs, foetus increases secretion of insulin.

Once isolated from other, neonate experiences reflex due to hgih circulating levels of insulin, can damage brain due to hypoglycaemia.

47
Q
A