Interpreting lab tests
Interpreting common lab tests: FBC, LFTs, renal, coagulation, ABG, urine and CSF
Normal ranges and classic patterns for blood count, iron studies, renal and liver tests, coagulation, blood gases, urine and CSF. Each pattern is explained by its physiology so you can read results you have not memorised.
Blood count and red cell indices
| Test | Normal adult range | Key interpretation |
|---|---|---|
| Haemoglobin | Men 13–17 g/dL; women 12–15 g/dL | Anaemia below 13 (men), 12 (women), 11 in pregnancy |
| MCV | 80–100 fL | Microcytic: iron deficiency, thalassaemia, anaemia of chronic disease, sideroblastic, lead. Macrocytic: B12 or folate, alcohol, liver disease, hypothyroidism, reticulocytosis, methotrexate, hydroxyurea |
| WBC | 4–11 × 10^9/L | Neutrophilia in bacterial infection and steroids; lymphocytosis in viral infection and CLL |
| Platelets | 150–400 × 10^9/L | Spontaneous bleeding below about 20; surgery usually safe above 50 |
| Reticulocytes | 0.5–2.5% | Reflect marrow output. A count of 8% means the marrow is responding to haemolysis or bleeding; it also rises within days of giving iron to a deficient patient. Low in marrow failure |
- Pregnancy: plasma volume rises about 50% but red cell mass only about 25%, so Hb falls (for example 12.5 to 11 g/dL) with normal MCV and ferritin: physiological haemodilution.
- Beta-thalassaemia trait: very low MCV with near-normal Hb, raised HbA2 (over 3.5%), Mentzer index (MCV/RBC) under 13.
| Film finding | Points to |
|---|---|
| Target cells | Thalassaemia, liver disease, hyposplenism |
| Schistocytes | DIC, HUS, TTP, mechanical valves |
| Spherocytes | Hereditary spherocytosis, autoimmune haemolysis |
| Howell–Jolly bodies | Hyposplenism |
| Heinz bodies, bite cells | G6PD deficiency |
| Teardrop cells | Myelofibrosis |
| Hypersegmented neutrophils | B12 or folate deficiency |
| Smudge cells; Auer rods; rouleaux | CLL; AML; myeloma |
| Basophilic stippling | Lead, thalassaemia |
- ESR rises with myeloma, giant cell arteritis and polymyalgia (often over 100 mm/h), TB and infection; it is low in sickle cell disease and polycythaemia.
Iron studies and haemolysis
| Condition | Ferritin | Transferrin saturation | TIBC |
|---|---|---|---|
| Iron deficiency | Low | Low | High |
| Anaemia of chronic disease | Normal or high | Low | Low |
| Haemochromatosis | High | High (over 45%) | Low |
- Ferritin is an acute phase protein, so it also rises in inflammation; transferrin saturation separates iron overload from inflammation.
- Haemolysis: raised unconjugated bilirubin, LDH and reticulocytes; low haptoglobin.
- PNH: complement destroys red cells lacking the GPI-anchored protectors CD55 and CD59. Dark morning urine, pancytopenia and hepatic vein thrombosis (Budd–Chiari); confirm by flow cytometry for CD55/CD59 (or FLAER).
- HbA1c reflects glucose exposure over the red cell lifespan. Where lifespan is shortened (sickle cell, haemolysis, recent bleeding), HbA1c is falsely low; use glucose or fructosamine.
- ABO and Rh typing: red cells agglutinate with the antisera matching their antigens; plasma holds antibodies to the antigens the person lacks. Agglutination with anti-A and anti-D, with anti-B in the plasma, is group A Rh-positive.
Kidney, electrolytes and acid–base
| Test | Normal |
|---|---|
| Sodium; potassium | 135–145; 3.5–5.0 mmol/L |
| Urea | 2.5–7.8 mmol/L (about 15–47 mg/dL) |
| Creatinine | 60–110 µmol/L (0.7–1.2 mg/dL) |
| Bicarbonate; chloride | 22–29; 98–106 mmol/L |
| Calcium | 2.2–2.6 mmol/L (8.8–10.4 mg/dL), corrected for albumin |
- High urea:creatinine ratio: pre-renal AKI, upper GI bleed (digested blood protein), catabolism. Low urea: liver failure, malnutrition, pregnancy.
- Pre-renal versus ATN: urine sodium under 20 versus over 40 mmol/L; FENa under 1% versus over 2%; bland urine versus muddy brown granular casts.
- Uraemic pericarditis (chest pain, friction rub, very high urea) is an indication for urgent dialysis; minimise heparin because the effusion may be bloody. Other indications: refractory hyperkalaemia, acidosis, fluid overload, encephalopathy.
- Low calcium, high phosphate, high PTH: chronic kidney disease (secondary hyperparathyroidism) or pseudohypoparathyroidism (PTH resistance). Vitamin D status is measured as 25-hydroxyvitamin D, the storage form.
- Primary hyperaldosteronism (Conn adenoma): hypertension with low potassium, metabolic alkalosis and suppressed renin (high aldosterone:renin ratio). High renin with hypertension suggests renal artery stenosis.
- Thiazide hyponatraemia with hypovolaemia (Na 119, low osmolality): stop the thiazide, give isotonic saline, correct slowly.
- Hyperkalaemia (for example 6.7 mmol/L in a patient on ACE inhibitors or spironolactone) gives tall T waves then wide QRS and arrest.
- Diarrhoea loses bicarbonate and potassium: normal anion gap (hyperchloraemic) metabolic acidosis with hypokalaemia (for example Cl 112, K 2.5, anion gap 10).
| Renal tubular acidosis | Defect | Potassium | Urine pH | Stones |
|---|---|---|---|---|
| Type 1 (distal) | Cannot secrete H+ | Low | Cannot go below 5.5 | Yes (calcium phosphate) |
| Type 2 (proximal) | Cannot reclaim bicarbonate | Low | Can fall below 5.5 once bicarbonate is low | No |
| Type 4 | Low aldosterone effect | High | Below 5.5 | No |
- Cystinuria: autosomal recessive defect in proximal tubular reabsorption of the dibasic amino acids cystine, ornithine, lysine and arginine (COLA). Only cystine is insoluble, forming flat hexagonal crystals and stones; cyanide–nitroprusside test is positive.
- ABG normals: pH 7.35–7.45; PaCO2 4.7–6.0 kPa (35–45 mmHg); PaO2 over 10.6 kPa on air; HCO3− 22–26. Type 1 respiratory failure: PaO2 under 8 kPa with normal or low PaCO2; type 2: PaCO2 over 6.5 kPa. Expected PaCO2 in metabolic acidosis (Winter formula) = 1.5 × HCO3− + 8 ± 2 mmHg.
Liver tests and hepatitis serology
| Pattern | Findings |
|---|---|
| Hepatocellular | ALT and AST very high (viral, ischaemic, paracetamol) |
| Cholestatic | ALP and GGT high, conjugated bilirubin, pale stools, dark urine |
| Alcoholic | AST:ALT over 2, high GGT and MCV |
| Synthetic failure | PT/INR prolonged (best acute marker; explains bleeding in cirrhosis), low albumin (chronic), low platelets from hypersplenism |
| Isolated unconjugated bilirubin | Gilbert syndrome (rises with fasting) or haemolysis |
| Isolated ALP, normal GGT | Bone (Paget, metastases, growth) or placenta |
- Jaundice is visible above about 35–50 µmol/L (2–3 mg/dL); normal under 21 µmol/L (1.2 mg/dL).
- Anti-HCV positive with normal LFTs: antibody shows exposure, not current infection; next test HCV RNA by PCR. If PCR is positive, the patient has current (active) infection, chronic if it persists beyond 6 months, and needs genotype or pan-genotypic antiviral treatment.
Coagulation
| Test | Pathway | Prolonged by |
|---|---|---|
| PT/INR | Extrinsic (VII) and common | Warfarin, vitamin K deficiency, liver disease, DIC |
| APTT | Intrinsic (XII, XI, IX, VIII) and common | Heparin, haemophilia A and B, lupus anticoagulant, some vWD |
| Bleeding time | Platelet function | vWD, aspirin, uraemia |
| D-dimer | Fibrin breakdown | VTE, DIC, surgery; useful only to exclude VTE |
- DIC: low platelets and fibrinogen, long PT and APTT, high D-dimer, schistocytes. von Willebrand disease: long bleeding time and APTT, normal PT.
Other common tests
- Diabetes: fasting glucose 7.0 mmol/L (126 mg/dL) or more; random or 2-hour 11.1 mmol/L (200 mg/dL) or more; HbA1c 48 mmol/mol (6.5%) or more.
- Thyroid: TSH is the best screening test. Exogenous thyroxine gives high T4, suppressed TSH and low thyroglobulin.
- Pancreatitis: amylase or lipase over 3 times normal (lipase more specific; level does not reflect severity).
- Urine: red cell casts (glomerulonephritis), white cell casts (pyelonephritis), fatty casts (nephrotic), muddy brown casts (ATN); sterile pyuria (renal TB, stones, partly treated UTI).
| CSF | Cells | Protein | Glucose |
|---|---|---|---|
| Bacterial | Neutrophils | High | Low |
| Viral | Lymphocytes | Normal or mildly high | Normal |
| TB | Lymphocytes | Very high | Low |
- Pleural fluid: Light criteria (fluid:serum protein over 0.5, LDH over 0.6) define an exudate. Ascites: SAAG 11 g/L or more means portal hypertension; neutrophils over 250/µL mean spontaneous bacterial peritonitis.
- Pre-analytical errors: haemolysis (false high potassium, LDH, AST), delayed separation, EDTA contamination (high K+, low Ca2+), drip-arm samples.
Remember Reticulocytes measure marrow effort; ferritin measures stores but rises with inflammation; transferrin saturation settles overload.
Exam trap HbA1c is falsely low whenever red cells die early.
Exam trap A positive anti-HCV test is not active infection; confirm with HCV RNA.
How FCPS asks about this
- Hb falls in late pregnancy with normal MCV and ferritin: physiological haemodilution.
- Reticulocytes 8%: increased marrow output (haemolysis or bleeding).
- Haemochromatosis iron pattern: high transferrin saturation and high ferritin.
- Haemolysis, pancytopenia, hepatic vein thrombosis: PNH, confirmed by CD55/CD59 flow cytometry.
- Hypertension, weakness, low potassium, alkalosis, low renin: Conn adenoma.
- Hypokalaemia, urine pH never below 5.5, stones: type 1 distal RTA; hexagonal crystals with positive nitroprusside test are cystinuria.
- Uraemic pericarditis in ESRD: urgent dialysis; low HbA1c in sickle cell is from shortened red cell life.
Test yourself on this topic
5 of the 39 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A diabetic patient with sickle cell disease has an HbA1c much lower than expected from her glucose diary. Why?
Answer: Shortened red cell lifespan
HbA1c is haemoglobin glycated non-enzymatically in proportion to average glucose over the red cell lifespan (about 120 days, weighted to the last 6–8 weeks). Conditions that shorten red cell survival (haemolysis, sickle cell disease, recent blood loss or transfusion, splenomegaly) give falsely low values; iron deficiency and splenectomy can give falsely high values. Some haemoglobin variants interfere with assays. Fructosamine (2–3 weeks) or continuous glucose monitoring can be used instead. HbA1c 48 mmol/mol (6.5%) or more is diagnostic of diabetes.
HbA1c
- Reflects ~2–3 months (red cell life)
- Falsely low: haemolysis, sickle cell, blood loss, transfusion
- Falsely high: iron deficiency, splenectomy
- Diagnostic: ≥ 48 mmol/mol (6.5%)
Remember Short-lived red cells, short memory of glucose.
Why the other options are wrong
- HbS binds more glucose Not the explanation.
- HbA1c covers only a week It reflects about 2–3 months.
- Her diary must be wrong The test is unreliable here.
- High glucose destroys HbA1c Not true.
A young man has 2 days of headache, fever and neck stiffness but is alert. CSF: lymphocytes 150/µL, protein mildly raised, glucose 60% of blood glucose. What is the most likely diagnosis?
Answer: Viral (aseptic) meningitis
Viral meningitis (enteroviruses, HSV-2, mumps) gives a lymphocytic CSF with normal glucose and mildly raised protein, and the patient is usually not severely unwell. Bacterial meningitis gives neutrophils, very low glucose and high protein. Tuberculous and fungal meningitis give lymphocytes with low glucose and high protein over a longer course. Empirical antibiotics are started if bacterial meningitis cannot be excluded.
CSF patterns
- Viral: lymphocytes, normal glucose
- Bacterial: neutrophils, very low glucose
- TB: lymphocytes, low glucose, high protein
- Normal CSF glucose ~60% of blood
Remember Lymphocytes with normal sugar: viral.
Exam trap Early bacterial and partially treated meningitis can look lymphocytic.
Why the other options are wrong
- Bacterial meningitis Neutrophils and low glucose.
- Tuberculous meningitis Low glucose, high protein, subacute.
- Cryptococcal meningitis Low glucose; immunosuppressed; India ink.
- Subarachnoid haemorrhage Red cells and xanthochromia.
An elderly woman has a raised alkaline phosphatase with normal GGT, bilirubin and transaminases. What is the most likely source of the ALP?
Answer: Bone
ALP comes mainly from liver (biliary epithelium) and bone (osteoblasts), with smaller amounts from intestine and placenta (raised in the third trimester). A raised ALP with a raised GGT points to the hepatobiliary tree; a raised ALP with normal GGT points to bone: Paget disease (very high ALP, normal calcium), osteoblastic metastases (prostate), osteomalacia, healing fractures, hyperparathyroidism, and growing children. ALP isoenzymes can confirm the source.
Isolated ALP rise
- ALP + GGT ↑ → liver (cholestasis)
- ALP ↑, GGT normal → bone
- Bone causes: Paget, metastases, osteomalacia, growth
- Also: pregnancy (placental)
Remember GGT tells you whether ALP came from the liver.
Why the other options are wrong
- Bile ducts GGT would also be raised.
- Hepatocytes Transaminases would rise.
- Pancreas Not a source of ALP.
- Kidney Minor source.
A 50-year-old man has diabetes, skin bronzing, liver cirrhosis and arthropathy of the second and third MCP joints. Which iron study pattern is expected?
Answer: High saturation, high ferritin
Hereditary haemochromatosis (usually HFE C282Y homozygosity) increases iron absorption. Iron studies show raised serum iron, transferrin saturation over 45% (the earliest marker), high ferritin and low or normal TIBC. Iron deposits in liver, pancreas, skin, heart, pituitary and joints. Treatment is regular venesection. Anaemia of chronic disease gives low iron, low TIBC and normal or high ferritin.
Haemochromatosis
- HFE C282Y
- Earliest: transferrin saturation >45%
- High ferritin, low TIBC
- Diabetes, bronze skin, cirrhosis
- Treat: venesection
Remember Bronze diabetes with high saturation: venesect.
Exam trap Ferritin also rises in inflammation, so transferrin saturation is checked.
Why the other options are wrong
- Low ferritin, high TIBC Iron deficiency.
- Low iron and TIBC, high ferritin Anaemia of chronic disease.
- Entirely normal iron studies Not in this disease.
- Low ferritin and low saturation Iron deficiency.
A young man has recurrent kidney stones. Urine microscopy shows flat hexagonal crystals, and the cyanide–nitroprusside test is positive. Which transport defect is present?
Answer: Dibasic amino acid reabsorption
Cystinuria is an autosomal recessive defect of the transporter for the dibasic amino acids in the renal tubule and gut: cystine, ornithine, lysine and arginine (COLA). Cystine is poorly soluble in acidic urine and forms hexagonal crystals and radio-opaque stones. The nitroprusside test is positive. Treatment is high fluid intake, urinary alkalinisation and, if needed, penicillamine or tiopronin. Hartnup disease affects neutral amino acids.
Cystinuria
- Transporter for COLA amino acids
- Hexagonal crystals, stones
- Nitroprusside test positive
- Treat: fluids, alkalinise, penicillamine
Remember Hexagons in urine: cystine.
Exam trap Only cystine forms stones; the other three are soluble.
Why the other options are wrong
- Neutral amino acid reabsorption This is Hartnup disease.
- Phosphate reabsorption Phosphate wasting causes hypophosphataemic rickets.
- Glucose reabsorption by SGLT2 Glucose loss is renal glycosuria.
- Uric acid excretion Uric acid stones are radiolucent and not linked to this test.
Where this sits in the CPSP syllabus
- Paper 1: General pathology, Interpretation of common laboratory tests
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