Everything is significant in the case. While the text in the proposal is four and a half pages, the exhibits in the proposal are three pages. Since I've always thought of this as poetry, this economy of words and sparsity of style have always seemed to me to be like poetry. In addition, this brief, every-word-counts approach is not ideal; we usually strive for a more comprehensive treatment. In order to practice sorting what is important from what is unnecessary, we often include unnecessary or superfluous information. Instead, however, the style of Fabritek fits it quite well.

1 1. Why do conditions that cause retention of sodium, such as cardiac failure, result in low serum sodium? 2. What is meant by 'free water'?

2 Why is there a difference in the pattern of oedema in nephrotic syndrome and cardiac oedema? How is it related to the interstitial spaces and all that? I am confused.

3 Why is there a difference in the clinical presentation of oedema due to renal failure and oedema due to cardiac failure, and how is this related to the loose nature of the interstitial tissue in the periorbital area? The answer given was that it is because, in cardiac failure, there is orthopnoea and the most dependent portion in this case is the legs, which is why the oedema occurs there. You also mentioned that in renal failure there is no orthopnoea and the patient doesn't have to sit up, hence the difference. This does not seem to take into account right ventricular heart failure (RVF), where there is no question of orthopnoea. Pedal oedema is found in right ventricular failure. Is the answer not that, in congestive heart failure (CHF) there is pump failure (and the heart cannot pump blood against gravity) hence oedema in the dependent areas, whereas in renal failure there is no pump failure and the heart does not lose its capacity to pump blood against gravity. The oedema in this case develops in those tissues that have a loose interstitium, one such site being the periorbital area of the face. This is the reason for the difference in clinical presentation.

4 What treatment is recommended for recurrent attacks of generalized swelling, with angio-oedema, in a middle-aged female patient? 12 Water, electrolytes and acid-base

5 Is an osmotic diuresis, due to hyperglycaemia for instance, a cause of both hyponatraemia and hypernatraemia. Please explain how this can be the case.

6 What is the mechanism of 2-agonists (albuterol) in correcting hyperkalaemia in emergency? How does it cause a shift of potassium?

7 Why do we give sodium lactate along with sodium bicarbonate in acidotic patients? How does sodium lactate then act?

8 How does hypochloraemia alone cause a metabolic alkalosis?

9 I have read the part concerning acid-base imbalances and I would like to ask about two things: 1. Why is there a higher concentration of anions (18) on measuring the anion gap while there is a high concentration of immeasurable anions? I would have expected a higher concentration of cations because most of them are measurable. 2. Could you explain to me in more details how NaCO3 loss or HCl retention could lead to normal anion gap acidosis?

10 What is the exact formula for calculating the serum anion gap?