Explain ureteric flow, micturition, urine formation, normal urine constituents and defaecation.

Urinary Tract and GIT Physiology

Clinical Overview

Start with the single idea that makes everything else fall into place: the body is a bag of salt water, and two organ systems decide what comes in and what goes out. The kidney controls what stays in the blood and what leaves in the urine; the gut controls what enters from the outside and how fast it moves through. Almost every O&G problem in this chapter is a disturbance of one of those two ledgers, read against a pregnant baseline that has deliberately shifted.

Hold onto two more first principles and the rest is derivation. First, the kidney filters a huge volume and then claws almost all of it back — it makes about 170 litres of filtrate a day and returns roughly 99 percent of it, so the urine is the small, finely-tuned remainder. Second, pregnancy resets the thermostats: it filters more, dilutes the blood on purpose, relaxes smooth muscle everywhere, and slows the gut. A value that is "normal" in a non-pregnant adult can therefore be abnormal in pregnancy, and a symptom that would be trivial otherwise can be a clue to real disease.

This matters at the bedside because the same physiology explains why a pregnant creatinine should be low, why pyelonephritis is dangerous, why a labouring woman can become hyponatraemic, why epidural analgesia and perineal pain can cause postpartum retention, why reflux and constipation are so common, and why hyperemesis is more than "bad morning sickness".

The useful questions throughout are: what is the organ system trying to regulate, how does pregnancy change the baseline, and how should symptoms and investigations be interpreted without overcalling normal physiology or missing disease?

High-yield chains:

Early pregnancy vasodilatation -> increased renal plasma flow -> increased GFR -> lower urea and creatinine -> a "normal" non-pregnant creatinine may be abnormal in pregnancy.

Progesterone and uterine compression -> ureteric dilatation and urinary stasis -> vesicoureteric reflux risk -> cystitis can ascend -> pyelonephritis and sepsis.

Labour epidural, pain and perineal oedema -> reduced bladder sensation and outlet dysfunction -> overdistension -> detrusor injury -> postpartum retention and overflow.

Vomiting -> hydrogen and chloride loss -> metabolic alkalosis; poor intake -> ketosis; prolonged poor intake -> thiamine depletion -> dextrose before thiamine can precipitate Wernicke encephalopathy.

Progesterone smooth-muscle relaxation plus raised intra-abdominal pressure -> lower oesophageal sphincter failure -> reflux; slow colonic transit plus iron and reduced mobility -> constipation and haemorrhoids.

Core Knowledge

The Nephron: One Filter, Then a Long Reclaiming Tube

Before the regulation, the hardware. The working unit of the kidney is the nephron, and each kidney holds roughly a million of them. A nephron is simply a filter followed by a long tube that edits the filtrate. Understand the filter and the tube and the rest of renal physiology is bookkeeping.

The filter is the glomerulus — a tuft of capillaries fed by an afferent arteriole and drained by an efferent arteriole, so it is a portal system with an arteriole on each side. Plasma is pushed across a three-layer barrier into the cup-shaped start of the tubule (Bowman capsule). The barrier is what keeps blood cells and large proteins in the blood: the capillary endothelium, a basement membrane, and the podocyte epithelium. Two features of that barrier do almost all the clinical work. It is a size filter (red cells and most plasma proteins are too large to pass, so normal filtrate contains essentially no protein and no cells) and it is a charge filter (the barrier is negatively charged, so it repels negatively charged albumin even at the borderline of the size cut-off). When the barrier is damaged — as in glomerular disease or the endothelial injury of pre-eclampsia — both selectivities fail and protein leaks into the urine. This is why proteinuria is a marker of glomerular integrity, and why significant proteinuria in pregnancy is never dismissed.

The filtrate then runs down the tube. The proximal tubule reclaims the bulk of filtered water, sodium, bicarbonate, glucose and amino acids. The loop of Henle builds the salty medullary gradient that lets the kidney concentrate urine. The distal tubule and collecting duct do the fine-tuning of sodium, potassium, hydrogen ion and water under hormonal control. Sitting where the distal tubule touches its own glomerulus is the juxtaglomerular apparatus, the sensor that releases renin and links the single nephron to whole-body blood pressure. Keep this filter-then-tube map in mind; every disturbance below sits at one of these stations.

Renal Function from First Principles

With the hardware in place, name the job. The kidney maintains internal constancy while allowing intake and losses to vary. It regulates extracellular volume, osmolality, electrolytes, acid-base balance, waste excretion, blood pressure and endocrine functions such as renin, erythropoietin and active vitamin D production. In O&G, renal physiology becomes visible through urine output, creatinine, proteinuria, sodium, potassium, magnesium handling and fluid prescriptions.

Clearance is the bridge between the filter and the blood test. Clearance is the volume of plasma that the kidney completely strips of a substance per unit time. If a substance is freely filtered and then neither reabsorbed nor secreted by the tubule, its clearance equals the glomerular filtration rate (GFR) — the filtered volume per unit time, normally about 120 mL/min for both kidneys, around 10 percent lower in women than men even after adjusting for body surface area. The plasma constituent that comes closest to this ideal is creatinine, which is why creatinine clearance is the everyday estimate of GFR. Creatinine is useful because it is produced fairly steadily from muscle and cleared mainly by filtration, but it is not perfect: it is slightly secreted as well as filtered, and it is influenced by muscle mass, diet, exercise, assay and changing volume status. Pregnancy changes the baseline so much that a single "within laboratory range" creatinine can mislead.

Two related ideas explain why the kidney is hard to injure by simple hypotension. The filtration fraction is the proportion of the plasma reaching the kidney that is actually filtered (GFR divided by renal plasma flow, roughly 0.18 normally). When perfusion falls, the efferent arteriole constricts more than the afferent, so the filtration fraction rises and GFR is defended even as renal plasma flow drops. This autoregulation keeps urine flowing across a wide range of blood pressures — but it has limits, and in severe haemorrhage, sepsis or pre-eclamptic vasoconstriction those limits are exceeded and oliguria then acute kidney injury follow. It is also why drugs that block this efferent tone (such as ACE inhibitors and angiotensin receptor blockers) can drop GFR sharply and are avoided in pregnancy and in volume-depleted states.

Pregnancy Renal Adaptation

Renal adaptation begins early — in fact it begins before conception, during the luteal phase, and continues if the pregnancy establishes. Systemic vasodilatation lowers effective arterial resistance; renal plasma flow and GFR rise before the uterus is large. Renal plasma flow peaks at roughly 70-80 percent above non-pregnant levels in the second trimester before easing back towards term, and GFR rises by about half above baseline by the middle of the first half of pregnancy. The kidneys themselves swell, lengthening by around a centimetre. Later, the enlarging uterus compresses the collecting system and bladder. The result is a pregnancy kidney that filters more, dilutes more, excretes some solutes differently and sits downstream of a circulation prone to oedema. Reassuringly, this gestational hyperfiltration — unlike the hyperfiltration that precedes diabetic nephropathy — is not driven by a damaging rise in glomerular capillary pressure, so it does not injure the healthy kidney.