Why Blood Results Interpretation Is Examined
Data interpretation stations are a core component of modern OSCE circuits, appearing both as standalone stations (interpret these results) and embedded in clinical scenarios (you have just received these results — what do you do?). The skill is not memorising every possible cause of every abnormality — it is applying a systematic approach that ensures you never miss something important, present your reasoning clearly, and correlate findings with the clinical context.
💡 Tip
The three-step approach to any abnormal result:
- 1Identify the abnormality and quantify it (mild/moderate/severe)
- 2Correlate with the clinical context — does this fit?
- 3Act — what investigations or management does this trigger?
Full Blood Count (FBC)
The Normal Ranges (Adult)
| Parameter | Normal range | Note |
|---|---|---|
| Haemoglobin | Male: 130–180 g/L; Female: 115–165 g/L | |
| MCV | 80–100 fL | Mean corpuscular volume |
| White cell count (WCC) | 4–11 × 10⁹/L | |
| Neutrophils | 2–7.5 × 10⁹/L | |
| Lymphocytes | 1.5–4 × 10⁹/L | |
| Platelets | 150–400 × 10⁹/L |
Anaemia — Classify by MCV
🧠 Mnemonic
Anaemia classification by MCV:
Microcytic (MCV <80) — think iron:
- Iron deficiency (most common — heavy periods, GI loss, poor diet)
- Thalassaemia
- Anaemia of chronic disease (can be normocytic too)
- Sideroblastic anaemia
Mnemonic: ITAS (It Takes A Second)
Normocytic (MCV 80–100):
- Anaemia of chronic disease
- Haemolysis
- Acute blood loss
- Renal failure (↓ erythropoietin)
- Bone marrow failure
Mnemonic: AHARB — "A HARB of normocytes"
Macrocytic (MCV >100):
- B12 deficiency
- Folate deficiency
- Alcohol (direct effect on marrow, commonest cause of macrocytosis in UK)
- Hypothyroidism
- Myelodysplasia
- Drugs (methotrexate, hydroxyurea, azathioprine)
- Reticulocytosis (reticulocytes are large)
Mnemonic: BFAHMDR — "Big Fat And Huge, Mostly Drink Regularly"
Raised WCC
| Type | Likely cause |
|---|---|
| Neutrophilia (>7.5) | Bacterial infection, acute inflammation, steroids, MI, myeloproliferative disease |
| Lymphocytosis (>4) | Viral infection (EBV/CMV), CLL, pertussis |
| Eosinophilia (>0.5) | Allergy, asthma, parasitic infection, Churg-Strauss, Addison's |
| Monocytosis | TB, inflammatory bowel disease, CMV |
| Neutropenia (<2) | Viral illness, drug-induced (chemotherapy, clozapine, carbimazole), sepsis |
⚠️ Red Flag
Neutropenia + fever = medical emergency (neutropenic sepsis). Any patient with an ANC <0.5 and a temperature >38°C needs immediate blood cultures, broad-spectrum IV antibiotics (per local protocol), and urgent haematology review. Mortality is high if antibiotics are delayed.
Platelets
| Finding | Consider |
|---|---|
| Thrombocytopaenia (<150) | ITP, drug-induced (heparin — HIT, quinine), DIC, bone marrow failure, hypersplenism, TTP |
| Thrombocytosis (>400) | Reactive (iron deficiency, infection, post-splenectomy, inflammation), essential thrombocythaemia |
Urea and Electrolytes (U&E)
Normal Ranges (Adult)
| Parameter | Normal range |
|---|---|
| Sodium (Na⁺) | 135–145 mmol/L |
| Potassium (K⁺) | 3.5–5.0 mmol/L |
| Urea | 2.5–6.5 mmol/L |
| Creatinine | Male: 60–110 µmol/L; Female: 45–90 µmol/L |
| eGFR | >60 ml/min/1.73m² |
| Bicarbonate | 22–29 mmol/L |
Sodium
Hyponatraemia (<135 mmol/L):
Approach by volume status:
- Hypovolaemic (dehydrated): GI losses, Addison's, diuretics
- Euvolaemic: SIADH (most common in hospital), hypothyroidism, psychogenic polydipsia
- Hypervolaemic (oedematous): cardiac failure, cirrhosis, nephrotic syndrome
💎 Clinical Pearl
SIADH causes — remember with BUMPS:
- Brain (head injury, meningitis, encephalitis, stroke)
- Under general anaesthesia / postoperative state
- Malignancy (especially small cell lung cancer — ectopic ADH)
- Pulmonary (pneumonia, TB, abscess)
- Small molecule drugs (SSRIs, carbamazepine, opioids, NSAIDs)
Hypernatraemia (>145 mmol/L): Water deficit or excess sodium. Causes: diabetes insipidus (central or nephrogenic), inadequate fluid intake (elderly, unconscious patients), osmotic diuresis (hyperglycaemia).
Potassium
⚠️ Red Flag
Hyperkalaemia is a cardiac emergency. K⁺ >6.5 mmol/L (or any level with ECG changes) requires immediate treatment:
- 1Calcium gluconate 10ml 10% IV — membrane stabilisation (does not lower K⁺)
- 2Insulin + dextrose — drives K⁺ into cells
- 3Salbutamol nebuliser — drives K⁺ into cells
- 4Sodium bicarbonate — if acidotic
- 5Calcium resonium or dialysis — definitive removal
ECG changes in hyperkalaemia (in order of severity): peaked T waves → flat P waves → widened QRS → sine wave pattern → VF
Hypokalaemia (<3.5 mmol/L):
- Causes: vomiting/diarrhoea, diuretics (especially loop and thiazide), Conn's syndrome (hyperaldosteronism), refeeding syndrome, Cushing's
- ECG: flat T waves, U waves, prolonged QT, ventricular arrhythmias
Mnemonic for U waves: "U need more potassium" — U waves = hypokalaemia.
Renal Function
| Stage | eGFR (ml/min/1.73m²) | Clinical implication |
|---|---|---|
| G1 (normal) | ≥90 | Normal or hyperfiltrating |
| G2 (mild) | 60–89 | Mildly reduced |
| G3a | 45–59 | Drug dose adjustments begin |
| G3b | 30–44 | Avoid metformin, NSAIDs; LMWH dose ↓ |
| G4 | 15–29 | Pre-dialysis planning |
| G5 | <15 | Renal replacement therapy |
Pre-renal vs intrinsic renal failure:
- Pre-renal: urea:creatinine ratio >100:1 (urea disproportionately raised — urea is reabsorbed by the tubules when flow is low)
- Intrinsic: urea:creatinine ratio ~60:1 (both equally raised)
Liver Function Tests (LFTs)
Normal Ranges (Adult)
| Parameter | Normal range |
|---|---|
| Bilirubin | <21 µmol/L |
| ALT | 7–56 U/L |
| AST | 10–40 U/L |
| ALP | 30–130 U/L |
| GGT | Male: <65 U/L; Female: <45 U/L |
| Albumin | 35–50 g/L |
| Total protein | 60–80 g/L |
Pattern Recognition
| Pattern | Dominant abnormality | Consider |
|---|---|---|
| Hepatitic | ↑↑ ALT and AST | Viral hepatitis, drug-induced (paracetamol, NSAIDs, statins), alcohol, ischaemic hepatitis |
| Cholestatic | ↑↑ ALP and GGT | Biliary obstruction (gallstones, cholangiocarcinoma, PSC), drugs (co-amoxiclav), PBC |
| Mixed | Both raised | Many causes — use clinical context |
💎 Clinical Pearl
ALT vs AST: ALT is more specific for hepatocellular damage (it's predominantly hepatic). AST is less specific — it rises in cardiac muscle injury (MI) and skeletal muscle injury too.
AST:ALT ratio >2:1 in the context of alcohol use is consistent with alcoholic liver disease. A ratio >3:1 is highly suggestive. This is because alcohol depletes pyridoxine (B6), which is needed more for ALT synthesis than AST.
GGT is the most sensitive marker of alcohol use — it rises with regular drinking even without significant liver disease. It is also induced by drugs (phenytoin, carbamazepine, rifampicin).
Albumin is a marker of synthetic function — a low albumin in the context of liver disease means the liver can no longer manufacture protein. This is a sign of chronic liver failure, not acute injury.
Arterial Blood Gas (ABG) Analysis
The 5-Step Approach
Step 1 — pH: acidosis or alkalosis?
- Normal pH: 7.35–7.45
- pH <7.35 = acidosis
- pH >7.45 = alkalosis
Step 2 — pCO₂: respiratory component?
- Normal pCO₂: 4.7–6.0 kPa
- ↑ pCO₂ causes acidosis (respiratory acidosis — hypoventilation)
- ↓ pCO₂ causes alkalosis (respiratory alkalosis — hyperventilation)
Step 3 — Bicarbonate (HCO₃⁻): metabolic component?
- Normal HCO₃⁻: 22–29 mmol/L
- ↓ HCO₃⁻ causes acidosis (metabolic acidosis)
- ↑ HCO₃⁻ causes alkalosis (metabolic alkalosis)
Step 4 — Is there compensation?
- Respiratory acidosis → kidneys retain HCO₃⁻ (slow, takes days)
- Metabolic acidosis → lungs blow off CO₂ (fast, takes minutes)
- If compensated, the pH moves toward normal but does not fully normalise
Step 5 — Anion gap (in metabolic acidosis)
- Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻). Normal: 8–16 mmol/L
🧠 Mnemonic
High anion gap metabolic acidosis — MUDPILES:
- Methanol
- Uraemia
- DKA (diabetic ketoacidosis)
- Propylene glycol / Paraldehyde
- Isoniazid / Iron
- Lactic acidosis (most common in hospital — sepsis, ischaemia)
- Ethylene glycol
- Salicylates
Normal anion gap metabolic acidosis — HARDUP:
- Hyperchloraemia
- Addison's disease
- Renal tubular acidosis
- Diarrhoea (loss of HCO₃⁻)
- Ureteroenteric fistula / Ureteric diversion
- Pancreatic fistula
Four Patterns — Know These Cold
| Type | pH | pCO₂ | HCO₃⁻ | Common causes |
|---|---|---|---|---|
| Respiratory acidosis | ↓ | ↑ | Normal (acute) / ↑ (compensated) | COPD exacerbation, opioid OD, neuromuscular disease |
| Respiratory alkalosis | ↑ | ↓ | Normal (acute) / ↓ (compensated) | Hyperventilation, PE, anxiety, salicylate poisoning (early) |
| Metabolic acidosis | ↓ | Normal (acute) / ↓ (compensated) | ↓ | DKA, sepsis, renal failure, lactic acidosis |
| Metabolic alkalosis | ↑ | Normal (acute) / ↑ (compensated) | ↑ | Vomiting, diuretics, Conn's syndrome |
Oxygenation
- pO₂: normal on air ≥10.6 kPa. Hypoxaemia = pO₂ <8 kPa (=Type 1 resp failure) or pO₂ <8 kPa + raised pCO₂ (=Type 2 resp failure)
- Type 1 RF: pO₂ low, pCO₂ normal/low — V/Q mismatch, diffusion defect (PE, pneumonia, fibrosis, pulmonary oedema)
- Type 2 RF: pO₂ low, pCO₂ high — hypoventilation (COPD, neuromuscular disease, obesity hypoventilation, sedation)
Presenting Blood Results in an OSCE
"The FBC shows a haemoglobin of [X] g/L, which is [below / significantly below] the normal range, consistent with [mild/moderate/severe] anaemia. The MCV is [X] fL, indicating [microcytic/normocytic/macrocytic] anaemia. In the context of this patient's [clinical history], the most likely cause is [iron deficiency / B12 deficiency / etc]. I would like to confirm with [ferritin/iron studies/B12/folate] and I would [management plan]."
Common Examiner Follow-Up Questions
"You've been handed a VBG showing pH 7.28, pCO₂ 2.8 kPa, HCO₃⁻ 13 mmol/L, lactate 4.2 mmol/L — what does this show?"
"This is a metabolic acidosis — the pH is low, bicarbonate is low, and the CO₂ is also low, indicating respiratory compensation (hyperventilation blowing off CO₂). The raised lactate of 4.2 suggests lactic acidosis, most likely secondary to sepsis or poor tissue perfusion. I would calculate the anion gap to screen for other causes and initiate the Sepsis Six immediately."
"What is the difference between type 1 and type 2 respiratory failure?"
"Type 1 respiratory failure is defined as a pO₂ below 8 kPa with a normal or low pCO₂. It results from V/Q mismatch or diffusion failure — causes include pulmonary embolism, pneumonia, pulmonary oedema, and pulmonary fibrosis. Type 2 respiratory failure is defined as a pO₂ below 8 kPa with a raised pCO₂ above 6 kPa. It results from hypoventilation — causes include COPD exacerbation, neuromuscular disease, chest wall deformity, and sedative drug overdose."