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."
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