
By Ian M Symonds; Sabaratnam Arulkumaran; E M Symonds
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Extra resources for Essential obstetrics and gynaecology
Example text
The fall in systemic TPR is partly associated with the expansion of the vascular space in the uteroplacental bed and the renal vasculature in particular; blood flow to the skin is also greatly increased in pregnancy as a result of vasodilatation. The vasodilatation that causes the fall in TPR is not due to a withdrawal of sympathetic tone, but is hormonally driven by a major shift in the balance between vasoconstrictor and vasodilator hormones, towards the latter. The vasodilators involved in early gestation include circulating PGI2 and locally synthesised nitric oxide, and later, atrial natriuretic peptide.
Renal bicarbonate reabsorption and hydrogen ion excretion appear to be unaltered during pregnancy. Although pregnant women can acidify their urine, it is usually mildly alkaline. Both total protein and albumin excretion rise during pregnancy, to at least 36 weeks. Thus in late pregnancy, an upper limit of normal of 200 mg total protein excretion/ 24 h collection is accepted. Using dipsticks to assess proteinuria in pregnancy gives highly variable data. THE ALIMENTARY SYSTEM Gastric secretion is reduced in pregnancy and gastric motility is low, so gastric emptying is delayed.
By the end of the first trimester the increase in blood glucose following a carbohydrate load is less than outside pregnancy (Fig. 12). Pregnant 250 Plasma glucose 200 150 38 weeks 120 100 50 0 µu/mL retention of 3–5 mmol of sodium per day into the fetal and maternal stores. The total net sodium gain amounts to 950 mmol mainly stored in the maternal compartment. However, the plasma concentration of sodium falls slightly in pregnancy, because of the marked rise in plasma volume. A similar change occurs with potassium ions, with a net gain of approximately 350 mmol.