Y2 fetal physiology Flashcards

1
Q

O2 + glucose=?

A

= Energy+ Co2+ H2O

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2
Q

The placenta acts like a ?

A

Lung

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3
Q

How does oxygen travel from maternal circulation to fetal?

A

Due to saturation of O2 in fetal blood being lower following the fetus having higher amount of Hb and their haemoglobin is better at binding O2.. More O2/Hb and more Hb creates a higher “suction” of O2 in the fetus and so the gas exchange in the placenta occurs.

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4
Q

What is aerobic metabolism?

A

It is the process of O2 and glucose in the fetal tissues are consumed to produce energy with CO2 and H2O as waste products. The O2 is used to metabolise the glucose.
When CO2 and H2O are reabsorbed into the bloodstream, they divide into Hydrogen ion H+ and Bicarbonate ion HCO3-. H+ is buffered in Hb, HCO3- seeps in to extracellular fluid. (in the placenta this. H+ and HCO3- returns to CO2 and H2O and is transferred into the maternal blood stream, keeping the amount of H- at a manageable level.)

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5
Q

How is Ph measured

A

in the amount of H+ in the bloodstream

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6
Q

How is the fetus able to survive high levels of toxic H+?

A

Their Hb is able to buffer them and store them, keeping them from entering the cells, alongside placental deloading of these into maternal bloodstream.

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7
Q

A high amount of H+ give a Ph that is?

A

acidic, <7.. logarithmic scale so can escalate to toxic levels very quickly. A negative difference in a low Ph is significantly more sinister than a negative difference in a higher Ph due to the logarithmic scale.

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8
Q

CO2 is carried in the blood in the form of ?

A

H+ and HCO3-, very little is in the form of pure CO2

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9
Q

The amount of CO2 in the blood is often measured as

A

pCO2, partial pressure.. mmHg or KPa as units

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10
Q

Fetal blood coming into the placenta has realtively

A

Low Ph, low pO2, high pCO2

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11
Q

Normal gaseous exchange depends on

A

Normal perfusion of the uterus and the placental bed

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12
Q

What could be examples of poor perfusion of the uterus and placenta due to maternal factors?

A

Commonly High blood pressure, less common hypoxia (during convulsion etc.)

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13
Q

What could be examples of poor perfusion of the uterus and placenta due to uterine factors?

A

Contractions, chronic impairment of uteroplacental arteries (pre-eclampsia),

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14
Q

What could be examples of poor perfusion of the uterus and placenta due to placental factors?

A

Placental abruption (Shortly leads to fetal demise), reduced placental circulation (pre-eclamptic conditions)

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15
Q

What could be examples of poor perfusion of the uterus and placenta due to fetal factors?

A

commonly cord compression, not so common fetal bradycardia, fetal erythraemia >260 bpm, fetal anaemia (Rh- factor, parvovirus)

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16
Q

poor perfusion of the uterus and placenta lead to

A

Accumulation of CO2 and reduced supply of O2

17
Q

What is respiratory acidaemia?

A

Accumulation of CO2 causing acidaemia.

When CO2 in the form of H+ and HCO3- is not removed by the placenta as quickly as it is produced, causing a low Ph. BAD.

18
Q

Acidosis

A

Low Ph in blood and tissues

19
Q

Acidaemia

A

low Ph in blood

20
Q

Which is higher, maternal pO2 or fetal pO2?

A

maternal pO2

21
Q

Is fetal cardiac output greater or smaller than an adults?

A

4x greater/kg

22
Q

hypoxaemia

A

low pO2 in blood

23
Q

hypoxia

A

low oxygen level in fetal tissues

24
Q

In which four ways does the fetus tackle with acute hypoxaemia?

A
  1. preventative oxygen stores
  2. increased oxygen extraction
  3. Centralisation of blood flow
  4. Anaerobic metabolism
25
Q

What role do the catecholamines have in the fetus?

A

To induce preventative measures against hypoxia, levels go up during labour.

26
Q

How does the fetus cope with chronic hypoxaemia?

A

Reduce oxygen consumption through, reduction in growth (IUGR), and more acutely reduction in movement.
O2 usage is optimised through, increased levels of Hb and O2 extraction.
O2 redirected to brain, heart and adrenals, leaving less for skin gut and kidneys (leading to nec, oligohydramnios and asymmetrical growth.

27
Q

Polycythaemia

A

raised levels of haemoglobin Hb in the blood

28
Q

chronic hypoxaemia can lead to?

A

IUGR, reduced movements, polycythaemia, nec, oligohydramnios and asymmetrical growth

29
Q

Anaerobic metabolism

A

process of cells producing energy without O2 with lactic acid as a biproduct. glycogen> glucose= energy and lactic acid (lactate plus H+). Glycogen stores are used up leading to low sugar levels/ hypoglycaemia in the new born.

30
Q

Glycogen

A

long term store of carbohydrate, stored in myocardium and liver, need to be changed into glucose to be used.

31
Q

metabolic acidaemia

A

fall in Ph due to accumulation of lactic acid

32
Q

accumulation in CO2 leads to

A

respiratory acidaemia

33
Q

accumulation in lactic acid leads to

A

metabolic acidaemia

34
Q

What does the base deficit tell us?

A

How much of the buffers that are used up, high base deficit means metabolic acidaemia rather than respiratory. as most of this buffer has been used up.

35
Q

Base deficit

A

The amount of base/alkali that would have to be added to restore blood/ECF Ph to normal. Calculated from Ph and CO2. Measured in mmol/l. In the fetus/new born it is calculated on extracellular fluid rather than blood.

36
Q

How does the fetal blood Ph relate to maternal blood Ph?

A

fetal blood Ph correlate with maternal and usually sits around 0,1 units lower. It can therefor go up in 1st stage of labour (maternal hyperventilating) and down in 2nd stage (maternal metabolic acidaemia following strenuous muscle activity of the uterus). If the difference is larger, placental gas-exchange might be compromised.

37
Q

aerobic metabolism produces x times more energy as anaerobic metabolism

A

19 times