Which ONE of the following statements is TRUE regarding the anion gap (AG)?
Answer: B: The AG is the difference between the measured cations and the measured anions. To maintain electrical neutrality, the number anions must equal the number of cations. Hence, the difference between the two (i.e. the anion gap) is a measure of the unmeasured anions in plasma. AG = [Na+ ] –{[ HCO3 − ] + [Cl− ]}. The normal value is < 12 mmol/L and is composed of proteins (primarily albumin), phosphate and organic anions such as lactate. Albumin is the major unmeasured anion and contributes almost the whole of the value of the AG. A normally high AG acidosis in a patient with hypoalbuminaemia may appear as a normal AG acidosis. This is particularly relevant in severely unwell and intensive care patients where lower albumin levels are common.
Hypoalbuminaemic states must therefore be corrected for by adding 2.5 to the AG for every 10 g/L below the normal albumin level.
A reduced AG may be present in conditions of increased unmeasured cations such as calcium, magnesium and lithium. Additionally, positively charged proteins from multiple myeloma and polyclonal gammopathies can cause a reduced AG as can bromide and iodine toxicity.
Elevation of the AG is most commonly associated with a metabolic acidosis, however, is not exclusive to and may be seen with many acid–base disturbances. Metabolic and respiratory alkalosis may also elevate the AG. Generally however, if the AG is >30 mmol/L, than a metabolic acidosis is present. If the AG is <30 mmol/L, then approximately one-third of these patients will not have a metabolic acidosis. Therefore, an AG should be calculated in all acid–base disturbances.
References:
Which ONE of the following statements is FALSE regarding the delta gap?
Answer: D: The delta gap is a measure of the relationship between the anions in the blood and can be calculated as the ratio of the change in AG to the change in [HCO3 − ]. It can be used in the presence of a high AG metabolic acidosis to further evaluate for a coexistent metabolic abnormality. In a pure high AG metabolic acidosis the rise in the AG equals the fall in bicarbonate and there is a 1:1 relationship between the AG and the fall in bicarbonate. If the rise in the AG is less than the fall of the bicarbonate then a mixed high AG and normal AG metabolic acidosis coexist. If the rise in the AG is greater than the fall of the bicarbonate then a mixed high AG and metabolic alkalosis coexist.
Some general guidelines are listed in table below:
DELTA GAP MEASUREMENTS:
Based on: Brandis K. Acid-base physiology. Online. Available: http://www.anaesthesiaMCQ.com.
Which ONE of the following is a cause for metabolic alkalosis?
Answer: B: There are multiple causes for metabolic alkalosis, which can be remembered either as an increase in acid losses or increased bicarbonate retention. Causes include:
Adrenal insufficiency, acetazolamide and profuse diarrhoea are all causes of a normal AG metabolic acidosis.
Reference:
A 28-year-old man is brought into the ED with a Glasgow Coma Scale (GCS) of 12/15 and having ingested an unknown substance. His blood results are as follows:
Which ONE of the following drugs/poisons would NOT typically explain the above results?
Answer: A: The venous blood gas shows an acidaemia with low bicarbonate, therefore indicating a metabolic acidosis.
Therefore, the venous blood gas shows a high AG metabolic acidosis, with coexistent respiratory acidosis and high osmolar gap.
All of the above drug choices cause a high AG metabolic acidosis. Ethanol and acetone are also both exogenous agents that directly cause a high OG. Cyanide poisoning causes a severe lactic acidosis and hence can cause a high OG. Paracetamol in overdose does not typically cause a lactic acidosis unless ingested in doses large enough to cause severe hepatotoxicity and fulminant hepatic failure.
The causes of a high OG include:
Which ONE of the following is a cause of saline unresponsive metabolic alkalosis?
Answer: C: Metabolic alkalosis results from either a loss of hydrogen ions or a gain in bicarbonate. Bicarbonate and chloride ions are closely kept in homeostasis and therefore a change in concentration of one will readily alter the plasma concentration of the other. Metabolic alkalosis can be classified as being chloride responsive or chloride unresponsive, which assists in the approach to treatment. Conditions that produce chloride loss and fluid loss, such as vomiting, diarrhoea, diuretic therapy and cystic fibrosis reduce serum chloride concentrations and extracellular volume, leading to an increase in mineralocorticoid activity. This stimulates the kidney to reabsorb sodium and bicarbonate and secrete potassium and hydrogen ions leading to a hypochloraemic, hypokalaemic metabolic alkalosis that responds to normal saline (chloride responsive metabolic alkalosis). Urinary chloride is usually <10 mmol/L. Alternatively, other conditions causing mineralocorticoid excess, such as Conn’s syndrome, Cushing’s syndrome, adrenal hyperplasia and renal artery stenosis also produce a state of hyperaldosteronism, which also leads to a metabolic alkalosis and hypokalaemia. In these conditions, however, the extracellular volume is expanded and patients may often be hypertensive. The metabolic alkalosis in these patients is perpetuated by the hypokalaemia rather than the volume depletion and consequently is chloride resistant. Urinary chloride is generally >10 mmol/L.
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