Acid-base and electrolytes for NEET PG: six lab pictures and the number to read first

Answer: B. Patient 1, hyperchloraemic acidosis

Patient 1, hyperchloraemic acidosis. Diarrhoeal stool carries bicarbonate out, which lowers plasma bicarbonate directly. The body retains chloride to balance the charge, so chloride rises while the anion gap stays normal: exactly patient 1's column. Renal tubular acidosis gives the same normal anion gap picture, and the urinary anion gap helps tell the two apart.

Why the closest rival loses: patient 1 with a high anion gap (D) is the right patient with the wrong reading: patient 1's chloride is raised, not the gap. Patient 2 (A and C) has a widened gap and a normal chloride, which points to an unmeasured acid such as ketones. Chloride up, gap normal: diarrhoea. Gap up, chloride normal: an unmeasured acid.

Recallab question 55348 · Medicine › Electrolyte · reference: Harrison's Principles of Internal Medicine

Answer: D. The acid-base rows only

The acid-base rows only. The needle is in a superficial vein, not an artery. A peripheral venous sample tracks arterial acidity, carbon dioxide and bicarbonate closely enough to judge acid-base: the table shows their differences are narrow. Its oxygen is what one tissue bed left behind and has no fixed relation to the arterial value: the oxygen difference spans a wide range, so no single figure can be recovered from it.

Why the closest rival loses: acting on the whole panel (A) ignores the evidence in the table that one row behaves differently from the rest. Acting on none of it (B) throws away a usable acid-base reading and costs the patient a second needle. Correcting the oxygen row (C) does not work, because the table gives a range, not a constant. Venous blood answers the acid question; only an artery answers the oxygen one.

Recallab question 59012 · Biochemistry › Acid-Base & Clinical Biochemistry · reference: Harper's Illustrated Biochemistry

Answer: B. Pseudohyponatraemia from hyperlipidaemia

Pseudohyponatraemia from hyperlipidaemia. The calculated osmolality starts from the sodium, so it follows a low sodium down. The measured value is independent of it and depends on real particles. In patient 2 the measured value is normal, so the cells see a normal tonicity, and the creamy plasma layer shows what is displacing the water in that sample. In patient 1 the two values agree, so that sodium is genuinely low and must be treated.

Why the closest rival loses: inappropriate antidiuretic hormone secretion (C) and psychogenic polydipsia (A) are true dilutional states, which lower the measured osmolality; patient 2's is normal. Hyperglycaemic hyponatraemia (D) is out because the glucose is normal and a glucose load would raise the calculated value as well. Measure it before you treat it.

Recallab question 57255 · Medicine › Electrolyte · reference: Harrison's Principles of Internal Medicine

Answer: C. Patient 1

Patient 1. The kidney needs solute to excrete water. Urine can be diluted to about 50 to 100 mOsm/kg and no further, so the water cleared in a day is capped by the solute taken in that day. Beer supplies water and carbohydrate but very little salt or protein. Eating almost nothing, he can clear only a few litres before water is retained. His urine is maximally dilute and almost free of sodium. When food or saline restores solute, free water pours out and the sodium can climb too fast.

Why the closest rival loses: patient 4 (A) has equally dilute urine but eats normal meals; twenty litres a day of water overwhelms even a full solute intake. Patient 3 (B) is dry with concentrated urine and a low urine sodium, which is volume depletion. Patient 2 (D) has concentrated, sodium-rich urine despite a low sodium and a normal diet, which is inappropriate antidiuresis. No solute in, no water out.

Recallab question 57852 · Medicine › Electrolyte · reference: Harrison's Principles of Internal Medicine

Answer: B. A low urine potassium

A low urine potassium. A kidney that is working conserves potassium hard once the plasma level falls. Patient 1's urine potassium is low while the plasma level is low, which is that conservation, so the loss must be elsewhere, and the gut is the only other large route. Patients 2 and 3 are still pouring potassium into the urine, so the kidney is the leak.

Why the closest rival loses: a low bicarbonate (A) is present in patient 1 and fits intestinal fluid losses, but it only narrows the cause; the urine potassium locates the route. A high bicarbonate (C) belongs to patients 2 and 3, whose losses are renal. A high blood pressure (D) goes with patient 2's mineralocorticoid excess, a renal loss. Low in, low out means the kidney is innocent.

Recallab question 56451 · Medicine › Electrolyte · reference: Harrison's Principles of Internal Medicine

Answer: C. Starting the aldosterone antagonist

Starting the aldosterone antagonist. Aldosterone drives sodium reabsorption and potassium secretion in the collecting duct, and blocking its receptor removes the main route by which potassium leaves the body. The first three values are flat and the climb begins at the fourth month, which is when this drug was started; no other bar starts there. When a result and a prescription change on the same date, the prescription is the first suspect.

Why the closest rival loses: the enzyme inhibitor (B) does raise potassium, but it was running unchanged through three normal results. The loop diuretic (A) was started two months earlier and lowers potassium. A fall in kidney function (D) is excluded by the box recording an unchanged creatinine. Line the results up against the prescription dates.

Recallab question 56352 · Medicine › Electrolyte · reference: Harrison's Principles of Internal Medicine