Which ONE of the following would NOT cause a high AG metabolic acidosis?
Answer: C: Causes of high AG metabolic acidosis can be remembered either by the mnemonic (CATMUDPILES):
Or, alternatively, by dividing them into the groups defined by the cause:
Fanconi’s syndrome is a disease that affects the proximal tubules of the kidney, impairing the reabsorption of glucose, amino acids, bicarbonate, phosphate and uric acid. Different forms of the disease affect different functions of the kidney. The form that affects the reabsorption of bicarbonate produces renal tubular acidosis type 2 and hence causes a normal AG metabolic acidosis.
Reference:
Rapid overcorrection of hyponatraemia can lead to all of the following EXCEPT:
Answer: D: Complications developing from the treatment of hyponatraemia are uncommon but are more likely to occur in patients with chronic hyponatraemia. Central pontine myelinosis (CPM) (or osmotic demyelination syndrome) is a neurological condition that progressively develops over 3–5 days after the correction of sodium. It is thought to be caused by correction of sodium at a faster rate than what the brain can adapt to at the higher osmolality. Demyelination is seen in the pontine and extra-pontine sites on MRI. There is an increased risk of developing CPM if the hyponatraemia has been present for >48 hours. Additionally, alcoholics, malnourished and elderly patients are more susceptible to the disease.
CPM is characterized by neurological findings such as fluctuating level of consciousness, mutism, dysphagia, dysarthria, quadriparesis and seizures. Severe debilitation can ensue for several weeks and in many cases are permanent. Cardiac arrhythmias are typically not caused by a direct effect of rapid correction of hyponatraemia.
References:
Which ONE of the following conditions is a cause of hypocalcaemia?
Answer: C: Hypocalcaemia is defined as [Ca2+ ] of <2.0 mmol/L. The most common cause is post-thyroid or parathyroid surgery (hypoparathyroid states). It can also occur secondary to decreased calcium absorption (vitamin D deficiency, malabsorption syndromes), increased excretion (renal insufficiency, alcoholism, loop diuretics), endocrine disorders (Conn’s syndrome, pseudo-parathyroidism), drugs (multiple though note loop diuretics cause hypocalcaemia and thiazide diuretics cause hypercalcaemia) and conditions that sequester calcium into damaged cells (e.g. sepsis, trauma, acute pancreatitis, rhabdomyolysis).
In contrast, the most common causes of hypercalcaemia are hyperparathyroidism (primary, secondary and tertiary), malignancies (typically from the production of parathyroid hormone-related protein and bony metastases) and rarer causes (e.g. sarcoidosis, hyperthyroidism, Paget’s disease, adrenal insufficiency).
Which ONE of the following statements is FALSE regarding rhabdomyolysis?
Answer: A: Rhabdomyolysis is a syndrome characterised by injury to the skeletal muscle and release of intracellular contents. There are numerous causes of rhabdomyolysis; however, the common terminal event appears to be disruption of the Na-K ATPase and calcium pump, leading to increased intracellular calcium and muscle cell necrosis. Additionally, the calcium activates numerous intracellular proteases and the production of free radicals further leading to cell death. Some of the causes of rhabdomyolysis includes drug and toxin abuse (e.g. cocaine, amphetamines), trauma, sepsis, heat-related injury and strenuous physical activity. Complications of rhabdomyolysis include:
The most common metabolic abnormality is hypocalcaemia. It usually occurs early in the disease process and is caused by the deposition of calcium salts in necrotic tissue. It is generally asymptomatic. Later in the disease process, calcium is mobilised from the damaged necrotic muscles and hypercalcaemia can ensue.
Other electrolyte abnormalities include serum phosphate levels, which are initially elevated early in the disease course. Later, however, mild hypophosphataemia may be seen but rarely requires treatment.
Hyperuricaemia occurs especially in crush injuries due to the release of muscle nucleotides, which are then converted to uric acid in the liver. These levels usually correlate well with the serum CK levels.
Hyperkalaemia occurs in 10–40% of cases due to release of potassium from injured skeletal muscle. The presence of renal failure, however, appears to be the most important determinant of the degree of elevation of the potassium. Hyperkalaemia can be a significant complication causing cardiac arrhythmias if acute renal failure occurs.
A 35-year-old female presents with a prolonged seizure. Her initial ABG is as follows:
Which ONE of the following explains the above blood gas?
Answer: D: An acidaemia exists with a low HCO3 and high CO2 level suggesting either a metabolic acidosis or a respiratory acidosis as the primary disorder. The calculated expected CO2 if the primary process was a metabolic acidosis would be 31. The measure CO2 is 50, indicating a second process of a respiratory acidosis. Conversely, if the primary process was a respiratory acidosis, then the expected HCO3 would be 25.5.
Through both calculations, you can see that there is a dual process occurring with a coexistent metabolic acidosis and respiratory acidosis. Given the scenario, it is most likely that the metabolic acidosis is the primary process with a secondary respiratory acidosis.
The AG is calculated to be 144 – [98 + 15] = 31 (i.e. elevated). The delta gap can also be calculated as 31 – 12/ 24–15 = 2.1, thereby also indicating a coexistent process to the high anion metabolic acidosis.
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