MLT GlobeChemistry: Electrolytes & osmolality – page 3
77 Chemistry MCQs on Electrolytes & osmolality with answers and explanations.
A patient with SIADH is expected to have:
In SIADH, ADH excess causes water retention, hyponatremia and low plasma osmolality, while urine osmolality stays inappropriately high (often >100 mOsm/kg) with ongoing urine sodium excretion.
Serum sodium is 125 mmol/L with serum osmolality 300 mOsm/kg. This hyperosmolar hyponatremia is most likely due to:
Glucose draws water out of cells, diluting sodium while raising osmolality. SIADH, hypothyroidism and water intoxication give hypo-osmolar hyponatremia.
A heparinised blood gas sample for ionised calcium is left open to air. The result is expected to be:
Loss of CO2 raises pH, increasing calcium binding to albumin and lowering ionised calcium. Samples should be anaerobic, and liquid heparin excess can also lower results by binding calcium.
A patient with stage G5 chronic kidney disease typically shows:
Reduced phosphate excretion and low 1,25-dihydroxyvitamin D production lower calcium and raise phosphate, driving secondary hyperparathyroidism.
Hypomagnesemia most commonly contributes to which other electrolyte problem that fails to correct with replacement alone?
Magnesium deficiency increases renal potassium loss, so hypokalemia is resistant until magnesium is corrected. It also impairs PTH secretion, causing hypocalcemia.
Which method is commonly used for serum magnesium on automated analysers?
Magnesium forms coloured complexes with calmagite or xylidyl blue. o-Cresolphthalein complexone is used for calcium, molybdate for phosphate and bromcresol green for albumin.
A patient with prolonged vomiting is most likely to show:
Loss of gastric HCl produces metabolic alkalosis with low chloride; volume depletion activates aldosterone, increasing renal potassium loss.
A patient with polyuria has no rise in urine osmolality after water deprivation. After desmopressin, urine osmolality still does not rise. This is most consistent with:
In nephrogenic DI the kidney does not respond to ADH, so neither dehydration nor desmopressin concentrates the urine. In central DI, urine osmolality rises clearly after desmopressin.
A 45-year-old with resistant hypertension has K 3.0 mmol/L and bicarbonate 32 mmol/L. Which is the recommended screening test for the suspected cause?
Hypertension with hypokalemia and metabolic alkalosis suggests primary aldosteronism; a high aldosterone with suppressed renin gives a raised aldosterone-to-renin ratio. Metanephrines screen for pheochromocytoma.
A patient with hypokalemia has a 24-hour urine potassium of 10 mmol/day. This most suggests potassium loss through the:
When potassium is lost outside the kidney, the kidney conserves it and urine K falls below about 20 mmol/day. Diuretics, mineralocorticoid excess and RTA all cause inappropriately high urine K.
A patient with diabetic ketoacidosis has K 5.2 mmol/L on admission. After IV insulin, K falls to 3.1 mmol/L. The main reason is:
Insulin stimulates Na/K-ATPase, moving potassium into cells; correcting acidosis adds to this shift. Total body K is usually low in DKA, so plasma K falls quickly once insulin is given.
A child has a sweat chloride of 72 mmol/L collected by pilocarpine iontophoresis. This result is:
Sweat chloride of 60 mmol/L or more is consistent with cystic fibrosis; 30–59 mmol/L is intermediate and below 30 mmol/L is unlikely. CF is caused by a defective CFTR chloride channel.
As blood passes through tissue capillaries, bicarbonate leaves the red cells. To keep electrical neutrality, which ion moves into the red cells?
This is the chloride (Hamburger) shift: bicarbonate formed by carbonic anhydrase moves out of the RBC and chloride moves in, which is why venous RBCs contain more chloride.
A patient with profuse diarrhea has Na 138, Cl 115 and HCO3− 14 mmol/L. Which disorder is present?
Anion gap = 138 − (115 + 14) = 9 mmol/L, which is normal. Bicarbonate lost in stool is replaced by chloride, giving a hyperchloremic normal anion gap acidosis.
Two days after total thyroidectomy, a patient has tingling around the mouth. Which laboratory pattern is expected?
Accidental removal or injury of the parathyroid glands causes hypoparathyroidism: low PTH, low calcium and high phosphate because PTH normally promotes phosphate excretion. High PTH with low calcium suggests secondary hyperparathyroidism.
Why are ionized calcium samples collected in syringes with "balanced" (calcium-titrated) heparin?
Unbalanced heparin binds free calcium, especially at high heparin concentration, causing falsely low ionized calcium. CO2 loss is prevented by anaerobic handling, not by the type of heparin.
Long-term use of which drug class is well known to cause hypomagnesemia?
Proton pump inhibitors can reduce intestinal magnesium absorption and cause severe hypomagnesemia after months of use. Potassium-sparing diuretics tend to conserve magnesium.
A woman with pre-eclampsia on IV magnesium sulfate develops loss of deep tendon reflexes and slow breathing. Which result is most likely?
Magnesium sulfate therapy can cause magnesium toxicity; loss of reflexes and respiratory depression appear as serum Mg rises well above the therapeutic range. Serum Mg should be checked urgently.
A severely malnourished patient is started on high-calorie feeding. Two days later there is muscle weakness. Which electrolyte fall is most characteristic of this refeeding syndrome?
Insulin released with carbohydrate feeding drives phosphate (with K and Mg) into cells for ATP synthesis, causing marked hypophosphatemia. It is the hallmark lab finding of refeeding syndrome.
A patient with a psychiatric illness has serum Na 124 mmol/L and urine osmolality 70 mOsm/kg. The most likely cause is:
Very dilute urine (below about 100 mOsm/kg) shows ADH is properly suppressed, so hyponatremia results from excess water intake. In SIADH urine is inappropriately concentrated.