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					Case study 1 A patient unconscious after a stroke is maintained on intravenous fluids for two days. What fluids and electrolytes would this patient need over these two days? How would you monitor fluid excretion and acid base balance? After two days he is still unconscious and you decide to feed the patient via a nasogastric tube. What do you understand by the term nitrogen balance? How would your prescribed feeding regime sustain normal nitrogen balance in this patient? Maintenance of fluid, electrolyte and pH balance would be crucial in an unconscious patient, even if renal function is normal. This would involve measuring urine fluid output, plasma levels of Na+, K+, HCO3-, Cl- and plasma pH at regular intervals and correcting where necessary with additions of the appropriate ion to the intravenous fluid or drug treatment to modify excretion patterns. Intravenous fluid input should match renal output. Deviations of acid-base balance (assessed by laboratory analysis of plasma pH and PCO2, from which bicarbonate level is computed [Henderson-Hasselbalch equation]) can be corrected with either bicarbonate (for acidosis) or ammonium chloride (for alkalosis). K+ status is particularly important since nerve and muscle excitability is dependent on ECF [K+]. Cardiac arrhythmia for example may result from deviations in [K+] homeostasis. Plasma [K+] also influences renal proton secretion and vice versa. Nitrogen balance is the difference between intake of nitrogenous compounds (mainly protein) and urinary excretion of the end products of metabolism of nitrogenous compounds (mainly urea). For an adult these two should be equal. A negative nitrogen balance (when excretion > intake) means that there is a net loss of tissue protein. For a patient who is being fed solely by intravenous infusion, maintenance of nitrogen balance requires provision of adequate amounts of amino acids in the intravenous fluid – and especially adequate amounts of the essential amino acids. (Think about why the N must be provided as amino acids, and not as protein if it is to be administered intravenously!) Case study 2 A patient with excessive alcohol consumption and liver disease (for example cirrhosis) has a serum albumin level of 18 g/l and a plasma ammonia level of 120 µmol/L. He is drowsy and confused. Explain the likely reason for low albumin; does the low albumin matter? Where does the ammonia come from and what should have happened to it? Could his drowsiness and confusion be related to these findings? Serum albumin is synthesised in, and secreted by, the liver. In liver disease the synthesis of various liver proteins will be impaired, and there will therefore be lower than normal secretion of proteins such as albumin. The breakdown of albumin (and hence the amount that must be synthesised for replacement) will be more or less normal, because most albumin breakdown occurs as a result of secretion into the gastro-intestinal tract and digestion in the gut lumen. A significant amount of ammonia enters the hepatic portal circulation from the large intestine, where it is formed by intestinal bacterial metabolism. A major source of ammonia in the gut lumen is urea, which diffuses from the bloodstream, and is hydrolysed to ammonia and carbon dioxide by bacterial urease. Although the bacteria use much of this ammonia for their own metabolism, a great deal is also absorbed. Normally the liver removes essentially all of the ammonia entering from the portal vein before blood leaves into the peripheral circulation. Some is incorporated into glutamate and glutamine (and thence into a wide variety of amino acids and other nitrogenous compounds); the remainder is mainly incorporated into urea. In cirrhosis there is impairment of normal blood flow through the liver (as a result of fibrosis), and a number of portal-caval anastomoses develop, so that some portal blood bypasses the liver and enters the vena cava directly. This means that a considerable amount of ammonia enters the peripheral circulation.

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Normal blood ammonia is <40 µmol/L; an increase to only about 100 µmol/L can lead to disturbance of consciousness. This is far too little to have any effect on blood pH. The main problem of elevated blood (and hence tissue) ammonia is the reaction of glutamate dehydrogenase – as tissue levels of ammonia increase, so the enzyme catalyses synthesis of glutamate, at the expense of α-ketoglutarate. This leads to depletion of α-ketoglutarate, and hence impaired activity of the citric acid cycle. The result of this is impaired formation of ATP, leading to impaired CNS function.

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