General (internal) medicine - clinical sciences and core topics
This domain tests whether you can apply physiology and pharmacology at the bedside: interpret an arterial blood gas, explain a mechanism, and choose the single next investigation rather than recite a list.
Acid–base in four steps
- Calculate the anion gap: Na − (Cl + HCO3). Correct for albumin by adding 2.5 mmol/L for every 10 g/L the albumin sits below 40 g/L.
- Check respiratory compensation with Winter's formula: expected pCO2 = 1.5 × HCO3 + 8 ± 2.
- Delta ratio = ΔAG ÷ ΔHCO3 (normal AG ≈ 12). A ratio <1 implies a coexisting normal-anion-gap acidosis; >2 implies a coexisting metabolic alkalosis.
- If hypoxaemic, calculate the A–a gradient and P/F ratio to separate shunt from hypoventilation.
Sodium and water
Assess volume status, urine osmolality and urine sodium together. Hypotonic hyponatraemia with urine osm <100 mosmol/kg suggests primary polydipsia; >100 with urine Na <30 suggests hypovolaemia; >100 with urine Na >30 suggests SIADH or a euvolaemic cause. Correct chronic hyponatraemia by no more than 8–10 mmol/L in 24 hours.
Pharmacology core
Loading dose = volume of distribution × target concentration; maintenance depends on clearance. Use adjusted body weight in obesity, and in liver disease trust albumin, bilirubin and INR over transaminases.
Worked example
pH 7.20, pCO2 24 mmHg, HCO3 9 mmol/L, Na 138, Cl 100, albumin 30 g/L. AG = 138 − 109 = 29; albumin-corrected AG ≈ 31.5, so ΔAG ≈ 19.5 and ΔHCO3 = 15, giving a delta ratio of 1.3 - a pure high-anion-gap acidosis. Expected pCO2 = 1.5 × 9 + 8 = 21.5 ± 2; the measured 24 sits at the limit, so compensation is adequate. Next step: lactate and ketones, not bicarbonate.
Traps
- Forgetting albumin correction and underestimating the anion gap.
- Labelling a primary respiratory alkalosis as compensation.
- Correcting sodium too rapidly, risking osmotic demyelination.
- Quoting a normal anion gap as proof that no acidosis exists when albumin is low.