Urine examination
Urine examination is one of simplest pro cedures which may disclose unsuspected dis ease processes
Collection: single random samples col lected in chemically clean containers are ad equate for routine analysis. Degenerative changes may develop on keeping the sample for some time & so fresh samples are preferred for routine microscopic examination. Morning sam ple is preferred for detection of pregnancy. For microbiological examination mid stream sam ple in sterile container is essential. If cytologi- cal examination for malignant cells is to be done centrifuged deposit from large volume of urine is preferred.
Physical examination
This includes colour, transparency, amount (volume), specific gravity and pH.
Colour: Normal urine is yellowish. The colour is darker with concentrated urine. Abnormal con- stituents may alter the colour. Blood, porphyrins and haemoglobin produce reddish orange col- our. Bile pigments produce yellowish green to brown colour Various drugs may change colour to yellow, orange, green or red.
Transparency: Normal urine is transparent. Pus cells & bacteria produce turbidity. Turbidity due to pus cells is removed by filtration while turbidity caused by bacteria persists after filtration. Crys tals (oxalates, phosphates, & urates) may pro duce turbidity. Fat & chyle impart respectively milky & cream colour to urine.
Volume : Normal daily 24 Hr. output in adults is usually 1000-1800 ml. Output less than 500 ml/ day is called oliguria. When it is < 100 ml/day the term anuria is used.
Increased urinary output (>2 litre/day)
called polyuria.
The commonest cause is Diabetes mellitus in which glucose in tubular lumen exerts osmotic effect inducing osmotic diuresis Polyuria is usually moderate in diabetes, about 5 litres urine being passed per day. Other causes of polyuria are diabetes insipidus, chronic renal failure, psychogenic polydipsia & diuretic therapy. In diabetes insipidus the polyuria is more severe (about 20 litres/day) & is due to failure of distal tubules in concentrating urine which leads to re duced reabsorption of water in distal tubules. This is due to deficiency of ADH normally secreted by posterior pituitary. In nephrogenic diabetes insipidus polyuria is again due to failure of tubu lar concentration mechanism but here ADH se- cretion is normal & the tubules fail to respond to ADH. In chronic renal failure the tubules them- selves are injured & also the nitrogenous sub stances (eg. urea) exert osmotic diuretic effect
leading to polyuria. Oliguria is commonly secondary to hypovolemia, renal diseases & conditions lead ing to generalised oedema like heart failure. Hypovolemia may be due to loss of fluid from various parts of body eg. GIT (vomiting, diar hoea), skin (prolonged high fever, burns), bleed ing from various parts of body due to injury/dis eases. Hypovolemia leads to reduced renal perfusion & increased reabsorption of water (1ADH & Taldosterone secretion) by kidney as a compenstory mechanism to save water & main tain volume. Renal diseases producing oliguria include acute glomerulonephritis (reduced GFR due to changes in glomeruli) & early stages of chronic renal failure.
Anuria deve ops when hypovolemia is extremne leading to shock, severe renal diseases (acute glomerulonephritis, acute tubular necrosis
