Physiology and pregnancy Flashcards

1
Q

What hormone drives maternal adaptations?

A

Progesterone

proactive changes rather then reactive, changes occur before necessarily needed

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2
Q

Give 3 reasons for adaptations observed in pregnancy:

A
  • Suitable environment for foetal nutrition, growth and development
  • Protect and prepare mother
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3
Q

What type of immunity is transfered to the foetus?

A

Passive immunity

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4
Q

What causes 40% of premature deliveries and why?

A

Maternal infections because mother has a suppressed immune state. Infections and parasitic diseases are more dangerous in pregnancy

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5
Q

What effect does pregnancy have on the mothers organs?

A
  • Thymus: shrink
  • Spleen: enlargement due to ^ erythrocytes and immunoglobulin producing cells
  • Para-aortic lymph nodes: enlargement as uterus drains here
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6
Q

Give 2 changes pregnancy causes to the uterus:

A
  • Myometrium growth due to muscle hypertrophy and elongation of cells
  • Vessel hypertrophy and ^ flow, trophoblast invasion of spiral arterioles (up to 24 weeks)
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7
Q

What prevents uterine contractility/ when do contractions start in pregnancy?

A

Progesterone prevents contractions.

Low level contractions start at week 7 (only contraction during labour cause cervical dilation)

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8
Q

What changes are undergone by the cervix during pregnancy?

A
  • Concentration of collagen reduces in third trimester
  • Increased vascularity
  • Antibacterial plaque of mucus forms
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9
Q

How much does CO increase by in the first trimester? By what degree does the heart rate increase by during pregnancy?

A

40%

15bpm

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10
Q

Why is heart disease a concern during pregnancy?

A

Due to higher CO during pregnancy, it could precipitate HF in those with underlying heart disease.

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11
Q

What allows the expansion of the mothers blood volume during pregnancy?

A

Reduction of total peripheral resistance by 1/2.

Caused by activation of RAS which ^ vasodilators

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12
Q

What effect does pregnancy have of BP?

A

Reduces mean arterial pressure (MAP) by about 10mmHg.

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13
Q

What happens with the 4th and 5th Korotkoff sounds during pregnancy?

A

Gap widens

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14
Q

What causes supine hypotension syndrome?

A

Compression of IVC in late pregnancy - decreased venous return

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15
Q

What should be done to ensure consistent accurate BP readings?

A

Measure BP in same posture each time

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16
Q

What effects does pregnancy have of RBC?

What happens to WBC numbers during labour and delivery?

A

Red cell mass ^ 20-30%
Haematocrit falls

Neurophil count ^^

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17
Q

What happens to a mothers lipid levels during pregnancy?

A

Hyperlidaemic state (but not atherogenic) - free fatty acids are raised

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18
Q

How does the volume of air inhaled and exhaled by a mother change during in pregnancy?
What happens to a mothers PaCO2 during pregnancy?

A

Volume ^ 40%.

PaCO2 falls (results in better gas exchange from foetus)

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19
Q

What happens to renal function and renal markers during pregnancy?

A

GFR ^

Plasma concentration of urea and CK fall

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20
Q

What is typical to observe on urine dip during pregnancy?

A

Glycosuria

Mild proteinuria

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21
Q

How does maternal weight change during pregnancy?

A

Total weight gain ~12.5kg (27.5 pounds)

  • 0.3kg/week up to 18weeks
  • 0.5kg/week up to 28 weeks
  • 0.4kg/week til term
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22
Q

What would too little or too much weight gain cause concern of?

A

Too much - investigate fluid retention

Too little - IUGR

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23
Q

List 4 breast changes noted in pregnancy:

A
  • Tenderness
  • increased size
  • Nipple enlargement (progesterone + prolactin)
  • Ductal proliferation (oestrogen, GH and glucocorticoids)
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24
Q

What hormone stimulates the production of cortisol?

A

ACTH

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25
Q

What are the levels of ACTH like during pregnancy?

A

High - so that more cortisol is produced

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26
Q

What does leucine aminopeptidase lower during pregnancy?

A

Oxytocin

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27
Q

What part of the pituitary releases prolactin?

A

Anterior pituitary

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28
Q

What does the posterior pituitary produce?

A

Oxytocin

ADH (antidiuretic hormone)

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29
Q

Why do some mothers experience constipation?

A

Due to increased water uptake from LI.

Enhanced nutrient uptake in SI is also experienced.

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30
Q

Where do placental villi form from?

A

Langhans cells

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31
Q

When does implantation of the blastocyst occur?

A

Day 7

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32
Q

What are stem villi called and what do they do?

A

They are maternal cotyledons and are formed 6 weeks after conception.
Functional part of placenta.

33
Q

Describe the structure of the umbilical cord and which direction they each run:

A

Umbilical Vein: goes from the mother, to the foetus (oxygen rich)

Umbilical arteries: Goes from foetus to the mother (oxygen poor)

There is a single umbilical vein from the placenta. Around this wraps TWO umbilical arteries going back to the mother.

34
Q

What surrounds the two umbilical arteries and the umbilical vein?

A

Whartons jelly. This is then covered in epithelium

35
Q

What should the full term foetal cord blood flow be?

A

350mL/min

36
Q

Describe the structure of chorionic villi:

A

Part of placenta that anchors into the endo/myometrium of the mothers uterus. Responsible for exchange between maternal and foetal circulation.

Maternal blood surrounds the chorionic villus whilst foetal blood runs through capillaries on the inside.

Exchange occurs across the syncytiotrophoblast cell layer (SYN)

37
Q

List 4 factors which can affect the foestal circulation:

A
  • Oedema of the cord
  • Intramural thrombosis (thrombi that adhere to the wall of a blood vessel
  • Calcification of large foetal vessels
  • Cord compression

(immediate and LETHAL consequences to foetus)

38
Q

List 4 acute factors which can affect uteroplacental circulation:

A
  • Maternal haemorrhage
  • tonic or abnormally long uterine contractions
  • Adrenaline and noradrenaline
  • Mother lying supine in late pregnancy (acute foetal asphyxia due to IVC compression)
39
Q

List 2 chronic pathologies which can affect the uteroplacental circulation:

A
  • Inadequate trophoblast invasion

- Acute atherosis of spinal arterioles

40
Q

List the main ways of transfer in the placenta:

A

1) simple diffusion - Oxygen, urea, fatty acids, ketone bodies
2) Facilitated diffusion - glucose transport
3) Active transport - Amino-acids and water-soluble vitamins
4) Transport of intact cells - an increased number of foetal cells in maternal circulation can suggest abortion/placental abruption

41
Q

List 3 functions of the placenta:

A

1) Gaseous exchange
2) Foetal nutrition and removal of waste
3) Plancental hormone production (endocrine function)

42
Q

Outline the endocrine function of the placenta:

A

Protein hormones:

  • hCG (maintains corpus luteum) peaks at 12 weeks
  • Human placental lactogen (unknown function)

Steroid hormones:

  • Progesterone - 17th week onwards
  • oestrogens (ovaries have little contribution)
  • Corticotrophin-releasing hormone (2nd + 3rd trimester)
43
Q

What is the normal range of birth weight?

A

2.7 - 4.1 kg ( 6-9 lbs )

44
Q

When does the heart beat typically present from?

A

4-5 weeks

45
Q

What is a typical CO at birth and at 2 months old?

A

Birth - 300-400ml/kg/min

2 months - 200ml/kg/min

46
Q

What are the two types of cells in the lungs and what do they each do?

A

Type 1 pneumocytes - gas exchange

Type 2 pneumocytes - surfactant production

47
Q

At what point during pregnancy is surfactant produced by? What are the two principal surfactants?

A

32 weeks

sphingomyelin and lechitin

48
Q

At what point in gestation are digestive enzymes present?

A

26 weeks

49
Q

At what point in gestation are foetal kidneys fully formed?

A

36 weeks

50
Q

What percentage of amniotic fluid is water?

A

99%

51
Q

In the second half of pregnancy, what becomes a significant contributor to amniotic fluid volume and why?

A

Foetal urine.

Onset of kidney function

52
Q

What is linked with impaired ability for the foetus to ingest amniotic fluid?

A

Congenital abnormalities

53
Q

What is the typical volume of amniotic fluid at 8, 38 and 42 weeks gestation?

A

8 weeks - 5-10mls
38 weeks - 1000mls
42 weeks - 300mls

54
Q

What can maternal diabetes cause a delay in?

A

Surfactant production

55
Q

What is lack of amniotic fluid known as?

A

Oligohydramnios

56
Q

What is too much amniotic fluid know as?

A

Polyhydramnios

57
Q

What 2 things may cause oligohydramnios?

A
  • Renal agenesis

- Growth restriction

58
Q

List 3 complication of oligohydramnios:

A
  • Pulmonary hyperplasia
  • Club foot
  • skull deformity
59
Q

What 3 things may cause polyhydraminos?

A
  • Maternal diabetes
  • Congenital abnormality
  • Multiple pregnancy
60
Q

List 3 complications of polyhydramnios:

A
  • Unstable lie (of baby)
  • Corp prolapse (through cervix)
  • Placental abruption
  • Post-partum haemorrhage
61
Q

List 4 things which can be detected on amniocentesis:

A
  • Help to detect chromosomal abnormalities (foetal karyotype)
  • Detect metabolic disorders
  • Detect foetal sex
  • Estimation of lung maturity where premature delivery is likely
62
Q

What is the action of oxytocin?

A

Milk ejection reflex

63
Q

What mobilises glucose from fat reserves, antagonises insulin, converts mammary gland into milk secreting tissue?

A

Human placental lactogen

64
Q

What medication is given to terminate a pregnancy?

A

Mifepristone (inhibits progestational hormones)

65
Q

At what point during the menstrual cycle is the endometrium ready for implantation?

A

20th-24th day

66
Q

What does a decline in Oestriol (E3) indicate during pregnancy?

A

Foetal distress. E3 is an indicator for foetal well being

67
Q

What cell do syncytiotrophoblasts and extra-villus trophoblasts derive from?

A

Cytotrophoblast (stem cell)

68
Q

Why is there no systemic immune response towards the foetus during pregnancy?

A

Syncytiotrophoblasts has no self/non-self markers which results in no T-/B-cell response.

Extra-villus trophoblast have modified self/non-self markers = modified maternal immune response

69
Q

Where do extravillous trophoblasts reside/ (draw a diagram)

A

Outside of the villous. These are found going into the maternal endometrium at the end of placental villi.

70
Q

Which antibody is able to cross the placenta and what diseases is it associated with?

A

IgG - Rhesus disease/haemolytic disease of the newborn

71
Q

Which antibody is secreted in breast milk?

A

IgA

72
Q

What cell type is responsible for Ig production?

A

B-Cells

73
Q

Explain rhesus factor and how it can cause issues in pregnancy:

A

No issues with primigravida. During labour of first pregancy baby and mums blood come into contact, mums B-cells start creating antibodies if baby is Rh+ve and mother is Rh-ve.

This then has impacts on later pregnancies. Mother has anti-Rh antibodies that can cross the placenta and attack blood cells of foetus which is Rh+ve

74
Q

What is given as prophylactic treatment for RhD? When is this this given?
Give two reasons why this is given:

A

Anti-D immunoglobulin

Either:

1) 1-dose in 28-30th week of gestation
2) 2-doses; one in 28th week and one in 34th week

  • Mother is Rh negative
  • If an invasive proceedure has been performed during pregnancy where foetal and maternal blood could mix (e.g. aminocentisis)
75
Q

What is chronic pregnancy vomiting known as?

A

Hyperemesis gravidarum

76
Q

What hormone can induce a insulin resistant state in mother during pregnancy and where is it made?

A

hPL - human placental lactogen. Produced by the synctiotrophoblast cells in the placental villi.

77
Q

Give a reason why maternal insulin resistance could be beneficial:

A

To spare glucose for the foetus

78
Q

What issues may maternal insulin resistance cause?

A

Causes glycogenolysis and gluconeogenesis = ^ in maternal free fatty acids and ketone bodies.
This in turn could produce diabetic ketoacidosis which needs to be controlled.

79
Q

List a cause of sub-optimal utero environement for each of the topics below - Psychiatric, endocrine, CV, resp, metabolic, reproductive:

A

Psychiatric - Schizophrenia

Endocrine - hypothyroidism

CV - CHD, stroke, HTN, pre-eclampsia

Metabolic - T2DM, insulin resistance

Reproductive - PCOS