1 1. One explanation is the non-osmotic release of antidiuretic hormone (ADH), due to arterial underfilling causing the retention of water and a dilutional hyponatraemia. A second explanation is that reduced delivery of chloride to the diluting segment of the ascending loop of Henle because of avid reabsorption of sodium and chloride in the proximal tubule. This results in a reduced ability to generate 'free water' and produce a dilute urine so hyponatraemia occurs due to water excess. 2. The term 'free water' is a concept that is used to describe the movement of water independent of sodium.

2 In all conditions associated with oedema there is increased extracellular volume associated with renal sodium chloride retention. The oedema in all conditions is usually in the ankles in all patients but this depends on body position. Patients with the nephrotic syndrome are not usually breathless and so lie flat and the oedema occurs in the face. The reverse is true for cardiac failure.

3 We are obviously going to disagree. Can we give you an example? In nephrotic syndrome, patients have periorbital oedema in the morning because of lying flat; in heart failure, the patient cannot lie flat because of orthopnoea. As oedema progresses, all spaces are eventually filled with fluid.

4 This sounds like idiopathic oedema of women. It might respond to diuretics. Antidiuretic hormone (ADH) acts on vasopressin (V2) receptors located on principal cells. ADH promotes water reabsorption in the collecting ducts and this might be a factor in the cause of the oedema. V2 receptor antagonists are now available. Further reading Hays RM (2006) Vasopressin antagonists - progress and promise. New England Journal of Medicine 355: 2146-2148.

5 Hypernatraemia is due to loss of Na and water with the osmotic diuresis. This causes dehydration and hypernatraemia. Hyponatraemia occurs because antidiuretic hormone (ADH) stimulates thirst; excess water compared to sodium is drunk, and hyponatraemia occurs.

6 2-adrenergic receptors increase the activity of the sodium-potassium ATPase pump in the cell membrane. This is followed by the excretion of excess potassium in the urine.

7 Sodium lactate intravenous infusion is obsolete for the treatment of metabolic acidosis. It carries the risk of lactic acidosis and should not be used.

8 If chloride is lost either through the kidney or via the stomach, there is a preferential absorption of bicarbonate in the distal tubule. This leads to metabolic alkalosis.

9 1. Normally there is an anion gap of approximately 12 mmol/L. Albumin normally makes up the largest portion of these unmeasured anions. 2. The loss of bicarbonate, e.g. from the gastrointestinal tract, is initially compensated but eventually the increased loss of bicarbonate leads to hydrogen ion excess;

10 Anion gap is calculated using serum concentrations as: (Na K)

(ClHCO3 ) The normal value is 6-12 mmol/L.