MRCPI GM Part I common mistakes
MRCPI GM Part I · Understand the traps and how to avoid them.
On ECG items, committing to a diagnosis from the overall 'pattern' after a few seconds' glance, without writing out rate, rhythm, axis, PR/QRS/QTc and a lead-by-lead ST-T analysis with reciprocal leads.
ECG teaching rewards gestalt recognition, and under time pressure the first familiar 'look' is accepted; subtle but decisive findings (posterior MI, left main occlusion, de Winter T waves, hyperkalaemia, long QT) are then missed.
What to do instead
Impose a fixed 30-second checklist before answering: rate, rhythm, axis, intervals (PR, QRS, QTc), hypertrophy, then ischaemia territory-by-territory with reciprocals; verbalise the derived findings even when the answer seems obvious.
Interpreting an arterial blood gas by reading pH, PaCO2 and PaO2 in isolation and labelling 'type 2 respiratory failure' or 'metabolic acidosis' without calculating expected compensation or the alveolar–arterial gradient.
Normal ranges are memorised but the compensation formulas and the alveolar gas equation are not, so a mixed disorder is reported as a single one and hypoxaemia is misattributed.
What to do instead
Apply Winter's formula for metabolic acidosis, the 1-for-0.7 and 4-for-2 rules for metabolic alkalosis, and check whether the measured PaCO2 matches the predicted value; calculate A–a gradient before calling hypoxaemia hypoventilatory.
Calling any raised ALT 'hepatocellular injury' and any raised ALP 'cholestasis' without calculating the R factor or checking whether the hyperbilirubinaemia is conjugated.
Single-enzyme pattern matching dominates revision, and mixed or infiltrative pictures (and an isolated ALP of bone origin) are then misclassified, sending the candidate to the wrong next investigation.
What to do instead
Calculate R = (ALT/ULN) ÷ (ALP/ULN): >5 hepatocellular, <2 cholestatic, 2–5 mixed; then choose the next test dictated by category (viral/autoimmune serology, ultrasound, MRCP) rather than repeating liver enzymes.
Diagnosing SIADH from a low serum sodium alone, without documenting serum osmolality <275 mOsm/kg, urine osmolality >100 mOsm/kg, urine sodium, clinical euvolaemia, and exclusion of hypothyroidism and adrenal insufficiency.
Hyponatraemia is revised as a list of causes with SIADH as the default label; the formal diagnostic criteria are rarely written out under exam conditions, and volume status is assumed rather than assessed.
What to do instead
Answer every hyponatraemia item in a fixed sequence: confirm true hypotonic hyponatraemia, assess volume status, then use urine osmolality and urine sodium; explicitly state which criteria are satisfied and which alternatives have been excluded.
Reporting the anion gap exactly as calculated from sodium, chloride and bicarbonate, without correcting for albumin and without calculating the delta ratio.
The uncorrected formula is what gets memorised, and hypoalbuminaemia - present in many of the clinical stems - masks a genuinely raised gap, so a high-anion-gap acidosis is called normal.
What to do instead
Corrected AG = measured AG + 2.5 × (4.0 − albumin); then compute the delta ratio (ΔAG ÷ ΔHCO3) to separate pure from mixed high-anion-gap acidosis, and calculate the osmolar gap where a toxic alcohol is possible.
Excluding stroke because a non-contrast CT performed within a few hours is normal, or labelling a deficit as anterior-circulation when the features (vertigo, diplopia, dysarthria, crossed signs, ataxia) are posterior.
CT is treated as a diagnostic test for ischaemia rather than a test that excludes haemorrhage, and posterior circulation syndromes are under-recognised because they are not the 'textbook' MCA picture.
What to do instead
Treat acute stroke as a clinical diagnosis built from onset time, deficit pattern and vascular territory; CT excludes haemorrhage only. For posterior features apply HINTS and proceed to MRI/DWI or CT angiography if doubt remains.
Treating a low MCV as iron deficiency and starting iron before checking ferritin with CRP and reviewing the blood film, so thalassaemia trait and anaemia of chronic disease are mislabelled and inappropriately iron-loaded.
Iron deficiency is the commonest cause and therefore the 'high-yield' answer; ferritin behaving as an acute-phase reactant, and the Mentzer index, are forgotten.
What to do instead
For microcytosis request ferritin with CRP (ferritin <15 µg/L diagnostic; <100 µg/L with inflammation supportive), a film, and the Mentzer index (MCV ÷ RBC >13 favours iron deficiency, <13 thalassaemia); check haemoglobin A2 before any iron loading.
Interpreting CSF white cell count, protein and glucose in isolation - concluding that a bland CSF excludes meningitis, or ignoring that antibiotics given before the lumbar puncture attenuate the CSF picture.
There is reflex recall of 'bacterial = neutrophils, viral = lymphocytes' without accounting for partially treated bacterial meningitis, TB/fungal disease or Listeria, and the drug history before LP is not sought.
What to do instead
Interpret the CSF as a whole against the clinical picture: use the CSF:blood glucose ratio and the published likelihood ratios for bacterial versus viral meningitis, always ask what antibiotics were given before the LP, and treat a suggestive clinical picture despite a normal CSF.
Answering interaction and prescribing items from a memorised list of drug names rather than from mechanism, so unfamiliar drugs or a new combination cannot be reasoned out and renal/hepatic dose adjustment is omitted.
Lists are quicker to cram than pathways, and question writers deliberately use agents outside the common list or add a comorbidity that changes clearance.
What to do instead
For each drug named, identify the metabolising enzyme and route of clearance, then ask three questions: does it change the concentration of the other drug, is toxicity additive, and does the eGFR or Child-Pugh score mandate dose reduction or avoidance?
Confusing sensitivity with positive predictive value - for example accepting that 'a highly sensitive test means a positive result is usually correct' - and answering screening items without reference to prevalence.
The 2×2 table is learned as a set of definitions rather than as a calculation, and prevalence, which drives PPV, is left out of the reasoning entirely.
What to do instead
For every test-characteristic item, draw a 2×2 table for a hypothetical 1000 patients at the stated prevalence, compute PPV and NPV from it, and state explicitly how a change in pre-test probability alters PPV while sensitivity and specificity stay constant.