22. Metabolic and Endocrine Control During Special Circumstances Flashcards

1
Q

What is the average weight gain during pregnancy?

A

About 8kg.

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2
Q

What are the two metabolic phases in pregnancy?

A

Anabolic phase - preparatory increase in maternal nutrient stores and increase in insulin sensitivity during early pregnancy.
Catabolic phase - decreased insulin sensitivity so increase in maternal glucose and free fatty acid concentration to allow for foetal growth in late pregnancy.

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3
Q

How are most substances transferred from mother to foetus?

A

By simple diffusion down concentration gradients.

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4
Q

How is glucose, the principal fuel, delivered to the foetus?

A

By facilitated diffusion through GLUT1 transporter primarily.

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5
Q

What is the new endocrine entity that develops during pregnancy?

A

The foetoplacental unit. It consists of the placenta, foetal adrenal glands and foetal liver.

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6
Q

What are two important placental steroid hormones?

A

Oestriol and progesterone.

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7
Q

What is the anabolic phase in pregnancy, during the first 20 weeks, in preparation for?

A

More rapid growth rate of the foetus, birth and subsequent lactation.

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8
Q

How is nutrient concentration kept high in maternal circulation during the second 20 weeks of pregnancy?

A

Reducing maternal utilisation of glucose by switching tissues to use of fatty acids, delaying maternal disposal of nutrients after meals and releasing fatty acid stores built up in the 1st half of pregnancy.

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9
Q

How does the insulin/anti-insulin ratio fall in the second half of pregnancy?

A

Because although insulin levels increase, anti-insulin hormones production by the foetal-placental unit increases more quickly.

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10
Q

What are three anti-insulin hormones in pregnancy?

A

Corticotropin releasing hormone, human placental lactogen and progesterone.

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11
Q

What is the overall blood glucose levels change in late pregnancy?

A

It’s about 10% lower.

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12
Q

How do oestrogen and progestones increase insulin synthesis and secretion?

A

They increase sensitivity of maternal pancreatic B-cells to blood glucose.

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13
Q

What are the three known causes of gestations diabetes?

A
  1. Autoantibodies similar to those in type I DM.
  2. Genetic susceptibility similar to maturity onset DM.
  3. B-cell dysfunction in setting of obesity and chronic insulin resistance (most common).
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14
Q

How many pregnancies are affected by gestational DM?

A

3-10%.

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15
Q

What effect on the pregnancy does gestational DM have?

A

Increased incidence of miscarriage, 4x higher incidence of congenital malformation, foetal macrosomia (large body), risk of shoulder dystocia (fat around shoulders meaning baby could get stuck during birth), hypertensive disorders of pregnancy - e.g. preeclampsia.

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16
Q

What affects whether a pregnancy will be affected by gestational DM?

A

The women’s starting point in terms of insulin resistance before pregnancy. If it was low originally, the peak in pregnancy may not take it over the threshold for gestational DM.

17
Q

What are some risk factors of gestational diabetes?

A

Maternal age over 25 years, BMI over 25kg/m2, race/ethnicity (more common in Asian, Black and Hispanic groups), personal or family history of DM and family history of macrosomia (large body).

18
Q

How is gestational DM managed?

A

Dietary modification (calorific reduction in obesity), insulin injection if persistent hyperglycaemia is present and regular ultrasound scans to assess foetal growth and well being.

19
Q

What must the metabolic response to exercise ensure?

A

The increased energy demands of skeletal and cardiac muscle are met by mobilisation of energy stores, minimal disturbances to metabolic homeostasis - keep rate of mobilisation = rate of utilisation, glucose to brain maintained and end products of metabolism are removed ASAP.

20
Q

What does the magnitude and nature of metabolic response to exercise depend on?

A

Type of exercise, intensity and duration of exercise and physical condition and nutritional state of individual.

21
Q

How much ATP is stored in muscle?

A

A limited amount, 5mmol/kg.

22
Q

Where does energy come from in exercise after muscle stores of ATP are used?

A

Muscle creatine phosphate stores replenish ATP for immediate energy.

23
Q

Beyond the initial burst of energy, where is further ATP supplied by?

A

Glycolysis and oxidative phosphorylation.

24
Q

What are two key differences between getting ATP from glycolysis and oxidative phosphorylation?

A

Glycolysis is inefficient but can be done anaerobically. Whereas oxidative phosphorylation is efficient but requires oxygen.

25
Q

What can intensive exercise by sustained by?

A

Muscle glycogen.

26
Q

What happens in the Cori cycle?

A

Lactate produced by the muscle is taken to the liver and converted to glucose. That glucose is taken back to the muscle, where is is metabolised to produce my lactate.

27
Q

How does muscle take up blood glucose?

A

Via GLUT4 and GLUT1 transporters.

28
Q

What happens to metabolism during a 100m sprint?

A

Not enough oxygen to muscles. High energy phosphate stores are used then ATP is created anaerobically (inefficient and incomplete metabolism of glucose). This produces lactate and causes fatigue. Muscle stores of glycogen are used.

29
Q

What happens to metabolism during a 1500m middle distance run?

A

Some extra oxygen is delivered to muscles. 40% anaerobic metabolism. Initial start - creatine phosphate and anaerobic glycogen metabolism. Middle phase - ATP produced aerobically from muscle glycogen. Finishing sprint - anaerobic metabolism of glycogen.

30
Q

What happens to metabolism during a marathon?

A

95% aerobic. Uses muscle glycogen, liver glycogen and fatty acids. The muscle glycogen stores are depleted within a few minutes and glucose from the liver peaks at about 1 hour and then decreases. Use of fatty acids rises steadily from 30 minutes.

31
Q

Order the following energy sources in the order they’d be used in exercise.
ATP, muscle glycogen (anaerobic), plasma free fatty acids, plasma glycogen, adipose tissue triglycerides, creatine phosphate, muscle glycogen (aerobic) and liver glycogen.

A

ATP and creatine phosphate.
Muscle glycogen (anaerobic).
Muscle glycogen (aerobic), plasma glycogen and liver glycogen.
Plasma free fatty acids and adipose tissue triglycerides.

32
Q

How is metabolic response to a marathon hormonally controlled?

A

Insulin levels fall slowly - inhibition of secretion by adrenaline.
Glucagon level rise - stimulates glycogenolysis (glycogen phosphorylase), gluconeogenesis (PEPCK and fructose 1,6 biphosphatase) and lipolysis (hormone sensitive lipase).
Adrenaline and growth hormones rise - stimulates glycogenolysis and lipolysis, mobilises fatty acids.
Cortisol slowly rises - stimulates gluconeogenesis and lipolysis.

33
Q

What are the benefits of exercise?

A

Body compositional changes - decreased adipose and increased muscle.
Glucose tolerance imporves - increased muscle glycogenesis.
Insulin sensitivity of tissues increases.
Blood TAGs decrease - reduced VLDL and LDL and increased HDL.
Bloody pressure falls.
Psychological effect - feelings of well being.