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Kofi: Pure Clinical Sem 3 > Repro: Pregnancy and Adaptation > Flashcards

Repro: Pregnancy and Adaptation Flashcards

1
Q

What is the week of 2’s?

A

Two distinct cell layers

Outer cell mass

  • Syncytiotrophoblast
  • Cytotrophoblast

Inner cell mass becomes the bilaminar disk

  • Epiblast
  • Hypoblast
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2
Q

What are 2 cavities in the embryo?

A
  • Amniotic cavity

- Yolk sac

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3
Q

How is the embryo suspended in the chorionic cavity?

A

-Connecting Stalk

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4
Q

What is the fate of embryonic spaces?

A
  • The yolk sac disappears
  • The amniotic sac enlarges
  • The chorionic sac is occupied by the expanding amniotic sac
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5
Q

What does implantation achieve?

A

Establishes the basic unit of exchange
-Primary villi: early finger-like projections of trophoblast
-Secondary villi: invasion of mesenchyme into core
-Tertiary villi: invasion of mesenchyme core by fetal vessels
Anchor the placenta
Establish maternal blood flow within the placenta

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6
Q

How does membrane change through pregnancy?

A
  • Implantation is interstitial (the uterine epithelium is breached and the conceptus implants within the stroma)
  • The placental membrane becomes progressively thinner as the needs of the fetus increase
  • In the human one layer of trophoblast ultimately separates maternal blood from fetal capillary wall (but the two circulations never mix)
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7
Q

What is a chorionic villus?

A

The placenta is a specialisation of the chronic villus. The chorion fondusum is the outer layer and has fingerlike projections. This allows finger-like projections from trophoblast that have vessels to allow for good exchange.

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8
Q

What are the possible implantation defects?

A
  • Impantation in the wrong place (Ectopic pregnancy, Placenta praevia)
  • Incomplete Invasion (Placental Insufficiency, Pre-Eclampsia)
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9
Q

Why is ectopic pregnancy bad?

A
  • No decidua therefore no control

- The conceptus can invade into tissues

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10
Q

How does the chorionic villus change from first semester to third semester?

A

First trimester - Thicker barrier

Third Trimester - Thinner barrier

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11
Q

What is the blood vessels to the umbilicus?

A
  • Two umbilical arteries to transport deoxygenated blood from foetus to placenta
  • Umbilical vein to transport Oxygenated blood from placenta to fetus
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12
Q

Which hormones are produced by the placenta?

A

Protein

  • Human chorionic gonadotrophin
  • Human chorionic somatomammotrophin
  • Human chorionic thyrotrophin
  • Human chorionic corticotrophin

Steroid

  • Progesterone
  • Oestrogen
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13
Q

What is hCG?

A
  • Hormone produced in the first 2 months of pregnancy
  • Supports secretory function of corpus luteum
  • Produced by syncytiotrophoblast therefore pregnancy specific
  • Excreted in eternal urine and therefore used as a basis for pregnancy testing
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14
Q

How do placental hormones influence maternal metabolism?

A
  • Progesterone increases appetite in order to lay down fat stores which will be called upon later in pregnancy
  • hCS/hPL increases glucose availability to fetus. Causes insulin resistance in maternal tissue so other stores are used by mother so the foetus gets glucose
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15
Q

What are transport functions of the placenta?

A
  • Simple diffusion (water, electrolytes, urea/uric acid, gases)
  • Facilitated diffusion (applies to glucose transport)
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16
Q

How does gas exchange occur in the placenta?

A
  • Simple diffusion
  • Diffusion barrier is small and decreases as pregnancy proceeds
  • Flow limited, not diffusion limited. Low stores of fetal oxygen so needs adequate low
  • Gradient of partial pressure is required so fetal pO2 must be lower than maternal pO2 which increases marginally.
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17
Q

Describe active transport in the placenta

A

Specific transporters expressed by syncytiotrophoblast for:

  • Amino acids
  • Iron
  • Vitamins
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18
Q

How does transfer of passive immunity occur?

A
  • Fetal immune system is immature
  • Receptor mediated process maturing as pregnancy progresses
  • Immunoglobulin class-specific
  • IgG only. Concentration in fetal plasma exceed this in maternal circulation
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19
Q

Why is the placenta not a true barrier?

A
  • Teratogens can access the fetus via the placenta
  • Unintentional outcomes from physiological process. Haemolytic disease of the newborn secondary to Rhesus incompatibility of mother and fetus. Can lead to destruction of metal erythrocytes. It can be prophylactically treated
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20
Q

What are examples of harmful substances and the placenta?

A
  • Thalidomide (Limb defects)
  • Alcohol (FAS and ARND)
  • Therapeutic drugs (anti-epileptic drugs, warfarin, ACE inhibitors)
  • Drugs of abuse (dependancy in the fetus and newborn)
  • Maternal smoking
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21
Q

What are the periods of susceptibility to teratogenesis?

A

Pre embryonic
-Lethal effects

Embryonic

  • More sensitive
  • Narrow windows for some systems

Fetal
+/- sensitive

After embryonic period, risk of structural defects very low
-Except CNS as development occurs throughout

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22
Q

What are the structures(vessels) of the maternal-fetal exchange that happens at the placenta?

A
  • Fetal circulation
  • Umbilical arteries (deoxygenated blood)
  • Umbilical vein (oxygenated blood)
  • Fetal capillaries within chorionic villi (increase surface area)
  • Uterine arteries
  • Uterine veins (maternal blood lakes in the intervillous spaces)
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23
Q

What factors increase fetal O2 content?

A
  • Fetal haemaglobin variant
  • Fetal haematocrit is increased over that in the adult
  • Increased maternal production of 2,3 DPG secondary to physiological respiratory alkalosis of pregnancy
  • Double Bohr effect
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24
Q

What is the fetal haemoglobin variant?

A
  • 2 alpha subunits plus 2 gamma subunits

- Greater affinity fo oxygen because it doesn’t bind 2,3-DPG as effectively as HbA

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25
Q

Describe the double Bohr effect in materno-fetal exchange.

A
  • As CO2 passes into intervillous blood, pH decreases
  • Bohr effect
  • Decreasing affinity of maternal Hb for O2
  • At the same time, as CO2 is lost, pH rises in the fetus
  • Bohr effect
  • Increasing affinity fo Hb for O2
26
Q

How does the concentration gradient for CO2 transfer form?

A
  • Maternal physiological adaptation to pregnancy
  • Progesterone-driven hyperventilation
  • Hence lower pCO2 in maternal blood
27
Q

What is the double Haldane effect?

A
  • As Hb gives up O2, it can accept increasing amounts of CO2
  • Fetus gives up CO2 as O2 is accepted
  • No alteration in local pCO2
28
Q

Describe the fetal circulation.

A
  • Receives oxygenated blood from mother via placenta in umbilical vein
  • Lungs are non functional so they are bypassed
  • Returns to the placenta via umbilical arteries
29
Q

What are the 3 shunts found in the fetal circulation?

A
  • Ductus Venosus
  • Foramen ovale (Right atrium to left atrium to by pass lungs)
  • Ductus arteriosus (pulmonary trunk to aorta)
30
Q

What is the purpose of the ductus venosus?

A
  • Connects umbilical vein carrying oxygenated blood to the IVC
  • Blood enters the right atrium so blood is shunted around the liver to maintain most of the saturation
31
Q

What is the purpose of the foramen ovale?

A
  • Right atrial pressure is greater than in the left atrium in the foetus
  • Forces leaves the foramen ovale part and blood flow into left atrium
  • Free border of septum secundum forms a crest
  • Creates two streams of blood flow
  • Majority of blood flow to Left atrium and the minor flows to Right ventricle
32
Q

Why is the ductus arteriosus needed?

A
  • Shunts blood from Right ventricle and Pulmonary trunk to Aorta
  • Minimuses drop in O2 saturation
33
Q

What is the fetal response to hypoxia?

A
  • HbF and Hb is increased
  • Redistribution of flow to protect supply to heart and brain
  • Fetal heart rate slows in response to hypoxia reduce O2 demand
34
Q

What is the effect of chronic hypoxaemia?

A
  • Growth restriction

- Behavioural changes

35
Q

How is hypoxia detected in the foetus?

A
  • Fetal chemoreceptors detect decreased pO2 or increased pCO2
  • Vagal stimulation then leads to bradycardia
36
Q

Which hormones are necessary for foetal growth?

A
  • Insulin
  • IGF1 and IGF2
  • Leptin
37
Q

What are the effects of nutrition on fetal growth during pregnancy?

A
  • Can cause symmetrical or asymmetrical growth restriction

- Can influence health in later life

38
Q

What is the dominant cellular growth mechanism in the first, second, and third trimester?

A

First trimester - Hyperplasia
Second trimester - Hyperplasia and Hypertrophy
Third trimester - Hypertrophy

39
Q

What is the purpose for amniotic fluid?

A
  • Amniotic sac encloses embryo/fetus in amniotic fluid
  • Protection
  • Contributes to development of lungs
40
Q

How is the amniotic fluid produced and recycled?

A
  • Fetal urinary tract produced urine by 9 weeks
  • Fetal lungs
  • Fetal GI tract (Swallowed and absorbs water and electrolytes. Debris and intestinal secretions accumulates in Gut to form meconium)
  • Placenta and fetal membranes
41
Q

What is the composition of amniotic fluid?

A
  • 98% water

- Plus electrolytes, cretinne, urea, bile pigment, renin, glucose, hormones and fetal cells, lung and Venice caseosa

42
Q

What is amniocentesis?

A
  • Sampling of amniotic fluid
  • Allows for collection of fetal cels
  • Useful diagnostic test
43
Q

How is the bilirubin metabolised in the foetus and why?

A
  • During gestation, clearance of fetal bilirubin id handle efficiency by the placenta
  • Foetus cannot conjugate bilirubin
  • Immaturity of liver and intestinal processes for metabolism, conjugation and excretion
  • Physiological jaundice common
44
Q

What is the pattern of growth during development?

A
  • Embryonic period is characterised by intense activity but absolute growth is very small
  • Growth and weight gain accelerate in fetal period

Embryo - Intense morphogenesis and differentiation; little weight gain; placental growth most significant
Early fetus - Protein deposition
Late fetus - Adipose deposition

45
Q

How do body proportions change during detail period?

A
  • At 9 weeks the head is approx half crown-rump length

- Thereafter, body length and lower limb growth accelerates

46
Q

What is an obstetric ultrasound scan?

A
  • Safe method that can be used early in pregnancy to calculate age. This can rule out ectopic and number of foetuses.
  • Routinely carried out at 20 weeks to assess fetal growth and fetal anomalies
47
Q

How is crown-rump length used to date the pregnancy?

A
  • Measured between 7 and 13 weeks to date the pregnancy and estimate delivery date
  • Scan at T1 also used to check location, number, viability
48
Q

How can the fetal age be estimated?

A
  • Last menstrual period (prone to inaccuracy)

- Development criteria

49
Q

How is biparietal diameter used to date the pregnancy?

A
  • Distance between the parietal bones of the fetal skull

- Used in combination with other measurements to date pregnancies in T2 and T3

50
Q

How is abdominal circumference and femur length to date the pregnancy?

A
  • AC and FL used in combination with biparietal diameter for dating an growth monitoring
  • Also useful for anomaly detection
51
Q

How are birth weight classified?

A

3500g - Average
<2500g - suspects growth restriction
>4500g - macrosomia (maternal diabetes)

52
Q

Why can babies have a low birth weight?

A
  • Premature
  • Constitutionally small
  • Suffered growth restriction
53
Q

Describe an overview of the development of the Respiratory system?

A
  • Lungs develop relatively late
  • Embryonic development creates only the broncho pulmonary tree
  • Functional specialisation occurs in the fetal period
  • Stage of development has major implication for pre-term survival. Terminal sac stage is crucial by 24 weeks
54
Q

Outline the stages of lung development.

A

Pseudoglandular Stage - Duct system (bronchioles) forms with the bronchopulmonary segment created during the embryonic period. (Wks 8-16)

Canalicular stage - Formation of respiratory bronchioles budding from bronchiole formed previously (Wks 16-26)

Terminal sac stage - Terminal sacs begin to bud from respiratory bronchioles. Differentiation of Type 1 and Type 2 pneumocytes. Surfactant. (Wks 26)

55
Q

How are lungs prepared to assume full burden at birth at T2 and T3?

A
  • Breathing movement to condition the respiratory musculature
  • Fluid filled (amniotic) which is crucial for normal lung development
56
Q

What is respiratory distress syndrome?

A
  • Insufficient surfactant production
  • Often affects infant born prematurely so if delivery pre-term in unavoidable then glucocorticoid treatment to increase surfactant production
57
Q

Describe an overview of the urinary system.

A
  • Fetal kidney function begins in week 10
  • Fetal urine is a major contributor to amniotic fluid volume
  • Fetal kidney fucntion is not necessary for survival but without it there is oligohydramnios
58
Q

What is the importance of amniotic fluid volume?

A

Oligohydramnios

  • Too little
  • Can cause placental insufficiency and fetal renal impairment

Polyhydramnios

  • Too much
  • Fetal abnormality due to inability to swallow so recycling process is implicated
59
Q

Describe the overview of nervous system.

A
  • First to being development and last to finish
  • Corticospinal tract required for coordinated voluntary movement being to form in the 4th month
  • Myelination of brain only begins in 9th month
60
Q

When does movement develop in the foetus?

A
  • No movement until after 8th week

- After large repertoire of movement develop to practise for post-natal life (suckling, breathing)

61
Q

What is quickening?

A
  • Maternal awareness of fetal movement from 17 weeks onwards
  • Low cost, simple method of antepartum fetal surveillance
  • Reveal those fetuses requiring follow-up

Kofi: Pure Clinical Sem 3 (44 decks)

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