Cardiovascular Journal of Africa: Vol 27 No 2 (March/April 2016)

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 27, No 2, March/April 2016

AFRICA

Pituitary gland

The pituitary gland enlarges in pregnancy and this is mainly due

to proliferation of prolactin-producing cells in the anterior lobe.

Serum prolactin levels increase in the first trimester and are 10

times higher at term. The increase in prolactin is most likely due

to increasing serum oestradiol concentrations during pregnancy.

Levels of follicle-stimulating hormone (FSH) and luteinising

hormone (LH) are undetectable during pregnancy due to the

negative feedback from elevated levels of oestrogen, progesterone

and inhibin.

Pituitary growth hormone production is decreased

but serum growth hormone levels are increased due to growth

hormone production from the placenta.

The posterior pituitary produces oxytocin and arginine

vasopressin (AVP). Oxytocin levels increase in pregnancy

and peak at term. Levels of antidiuretic hormone (ADH)

remain unchanged but the decrease in sodium concentration in

pregnancy causes a decrease in osmolality. There is therefore a

resetting of osmoreceptors for ADH release and thirst.

Glucose metabolism

Pregnancy is a diabetogenic state and the adaptations in glucose

metabolism allow shunting of glucose to the foetus to promote

development, while maintaining adequate maternal nutrition.

Insulin-secreting pancreatic beta-cells undergo hyperplasia, resulting

in increased insulin secretion and increased insulin sensitivity in

early pregnancy, followed by progressive insulin resistance.

Maternal insulin resistance begins in the second trimester

and peaks in the third trimester. This is the result of increasing

secretion of diabetogenic hormones such as human placental

lactogen, growth hormone, progesterone, cortisol and prolactin.

These hormones cause a decrease in insulin sensitivity in the

peripheral tissues such as adipocytes and skeletal muscle by

interfering with insulin receptor signalling.

The effect of

the placental hormones on insulin sensitivity is made evident

postpartumwhen there is a sudden decrease in insulin resistance.

Insulin levels are increased in both the fasting and postprandial

states in pregnancy. Fasting glucose levels are however decreased

due to:

•

increased storage of tissue glycogen

•

increased peripheral glucose use

•

decrease in glucose production by the liver

•

uptake of glucose by the foetus.

Insulin resistance and relative hypoglycaemia results in lipolysis,

allowing the pregnant mother to preferentially use fat for fuel,

preserving the available glucose and amino acids for the foetus and

minimising protein catabolism. The placenta allows transfer of

glucose, amino acids and ketones to the foetus but is impermeable

to large lipids. If a woman’s endocrine pancreatic function is

impaired, and she is unable to overcome the insulin resistance

associated with pregnancy then gestational diabetes develops.

Lipid metabolism

There is an increase in total serum cholesterol and triglyceride

levels in pregnancy. The increase in triglyceride levels is mainly as a

result of increased synthesis by the liver and decreased lipoprotein

lipase activity, resulting in decreased catabolism of adipose tissue.

Low-density lipoprotein (LDL) cholesterol levels also increase

and reach 50% at term. High-density lipoprotein levels increase

in the first half of pregnancy and fall in the third trimester but

concentrations are 15% higher than non-pregnant levels.

Changes in lipid metabolism accommodate the needs of the

developing foetus. Increased triglyceride levels provide for the

mother’s energy needs while glucose is spared for the foetus.

The increase in LDL cholesterol is important for placental

steroidogenesis.

Protein metabolism

Pregnant women require an increased intake of protein during

pregnancy. Amino acids are actively transported across the

placenta to fulfill the needs of the developing foetus. During

pregnancy, protein catabolism is decreased as fat stores are used

to provide for energy metabolism.

Calcium metabolism

The average foetus requires about 30 g of calcium to maintain its

physiological processes. Most of this calcium is transferred to the

foetus during the third trimester and is derived from increased

dietary absorption by the mother.

There is a decrease in total

serum calcium concentration during pregnancy. This is mainly

due to a decrease in serum albumin levels due to haemodilution,

resulting in a decrease in the albumin-bound fraction of calcium.

However the physiologically important fraction, serum ionised

calcium, remains unchanged.

Therefore maternal serum levels

of calcium are maintained during pregnancy and foetal needs are

met by increased intestinal absorption, which doubles from 12

weeks’ gestation. However the peak demand for calcium is only

in the third trimester. This early increase in calcium absorption

may allow the maternal skeleton to store calcium in advance.

Serum levels of 25-hydroxyvitamin D increase and this is

metabolised further into 1.25-dihydroxyvitamin D. The increase

in 1.25-dihydroxyvitamin D is directly responsible for the

increase in intestinal calcium absorption.

Increased calcium absorption is associated with an increase in

calcium excretion in the urine and these changes begin from 12

weeks. During periods of fasting, urinary calcium values are low

or normal, confirming that hypercalciuria is the consequence of

increased absorption.

Pregnancy is therefore a risk factor for

kidney stones.

Skeletal and bone density changes

There is controversy regarding the effect of pregnancy on maternal

bone loss. Although pregnancy and lactation are associated with

reversible bone loss, studies do not support an association between

parity and osteoporosis in later life.

Bone turnover is low in the

first trimester and increases in the third trimester when foetal

calcium needs are increased. The source of the calcium in the third

trimester is previously stored skeletal calcium.

A study of bone biopsies in pregnancy has shown a change

in the micro-architectural pattern of bone in pregnancy but not

overall bone mass.

The changes reflect the need for the maternal

skeleton to be resistant to bending forces and biochemical

stresses needed to carry the growing foetus.

Other musculoskeletal changes seen in pregnancy include:

•

exaggerated lordosis of the lower back, forward flexion of the

neck and downward movement of the shoulders