GC158 Point-of-care Testing (POCT)
Point-of-care testing is diagnostic testing performed at or near the site of patient care, outside the central laboratory, to provide rapid results that facilitate immediate clinical decision-making.
Point-of-Care Testing (POCT)
This lecture (GC 158) covers the principles, advantages, limitations, quality requirements, and clinical applications of Point-of-Care Testing (POCT) – laboratory tests performed at or near the site of patient care to enable rapid clinical decision-making. The lecture is Chemical Pathology-heavy and directly examinable in MCQ and SAQ formats. It connects to multiple other GC and CFB lectures: DM management (glucometers), pregnancy (urine hCG), drug screening, blood gas analysis, urine dipstick interpretation, and laboratory interferences.
Learning Objectives (Inferred from Slide Content)
- Define POCT and understand its rationale.
- List the general considerations for governance of POCT (SOP, training, QA, QC, EQA, documentation, maintenance, safety).
- Enumerate advantages and desirable characteristics of POCT devices.
- Know the common examples of POCT in clinical practice.
- Interpret urine dipstick results, including false positives/negatives.
- Understand the urine pregnancy test – mechanism, hCG variants, causes of elevated hCG, false positives.
- Understand the blood glucose meter – methods, interferences (GDH-PQQ problem), limitations at extreme values, and the critical rule of sending a confirmatory lab sample.
- Know the basics of POCT blood gas analysis – specimen handling, timing, avoiding pre-analytical errors.
- Know about drug-of-abuse testing as POCT.
"Any test performed at the time at which the test result enables a decision to be made and an action taken that leads to an improved health outcome." — Tietz (as cited in GC 158 slide) [1]
The CFB lecture (MED10) adds: "POCT is clinical laboratory testing conducted close to the site of patient care where care or treatment is provided. POCT provides rapid turnaround of test results, enabling prompt and timely instigation of appropriate patient management." [2]
Why does POCT exist?
Traditional central laboratory testing follows a long chain: clinician orders test → phlebotomy → specimen transport → specimen receipt/registration → analysis → result authorisation → result communication. Each step adds turnaround time (TAT). In time-critical situations (e.g., hypoglycaemia, DKA, acute MI, massive haemorrhage), waiting for central lab results may delay life-saving interventions. POCT collapses the chain by putting the test where the patient is.
Key Principle
The benefit of POCT is ONLY realised if the result is accurate and reliable. A fast but wrong result is worse than a slow correct one because it may lead to harmful clinical decisions.
The lecture explicitly lists these governance pillars [1]:
| Governance Element | Why It Matters |
|---|---|
| Standard Operating Procedure (SOP) | Ensures every operator performs the test identically – reduces inter-operator variability |
| Training and Certification | Non-laboratorians (nurses, doctors, patients) operate POCT devices; they need formal training to avoid pre-analytical and analytical errors |
| Quality Assurance (QA) | The umbrella term for all activities that ensure test quality |
| Internal Quality Control (IQC) | Running known-value control samples at regular intervals on the device to detect drift/malfunction |
| External Quality Assessment (EQA) | Blinded proficiency testing samples sent by an external body to compare your device's results against other sites – detects systematic bias |
| Documentation and Reporting | Results must be recorded in the patient record; traceability is critical for medicolegal and clinical continuity |
| Maintenance | Regular calibration checks, cleaning, battery/reagent replacement |
| Safety | Sharps disposal (lancets), biohazard handling (blood/urine), infection control |
Exam Trap
Students often forget that POCT devices require the same quality framework as central lab analysers. The fact that a test is "bedside" does NOT excuse it from IQC/EQA requirements.
3. Advantages of POCT
Lecture slide: "Benefit is based on the accuracy and reliability of the POCT results." [1]
| Advantage | Explanation |
|---|---|
| Reduced TAT | The single biggest selling point; enables real-time clinical decisions |
| Improved patient management | Faster diagnosis → faster treatment → better outcomes |
| Reduced administrative work | No paper/electronic requisition, no specimen labelling chain |
| Minimised delay in sample collection | Operator collects and tests simultaneously |
| Minimal sample requirement | Finger-prick capillary blood, urine drop – less painful, less volume |
| Reduced transport delay | No pneumatic tube / porter needed |
| Reduced registration delay | No lab log-in step |
| Reduced time entering complex facility | Bypasses multi-step automated analyser queue |
"Transportation – disconnection between time, individual, specimen, laboratory and physician" [1]
Traditional testing introduces a "disconnection": the specimen is separated from the patient and travels a physical and administrative journey. POCT keeps specimen and patient together.
| Feature | Why |
|---|---|
| Portable | Can go to bedside, ambulance, rural clinic |
| Dry, stable, unit-dose device | No liquid reagents to spill/expire; each test strip is self-contained |
| Robust (storage and usage) | Tolerates temperature variation, jostling |
| Simple to use | Non-lab staff can operate reliably |
| Concordant result with central lab | If results don't agree with the lab, POCT is clinically useless |
| Safely operated | Minimal biohazard risk |
| Built-in / integrated calibration / QC | Self-calibrating reduces operator steps and error |
| Ambient storage temp for reagents | No refrigeration needed → simpler logistics |
| Low instrument cost | Cost-effective deployment at scale |
| Record keeping | Electronic connectivity to hospital information system (HIS) for automatic result upload |
From the lecture slide [1]:
| POCT Device | Common Clinical Use |
|---|---|
| Blood gas analysers | ICU, ED, operating theatre – pH, pO₂, pCO₂, HCO₃⁻, lactate, electrolytes |
| Blood gas/electrolyte/metabolite handheld meters | Rapid K⁺ in hyperkalaemia, Na⁺ in hyponatraemia |
| Haemostasis analysers | ACT in cardiac surgery (heparin monitoring), TEG/ROTEM in massive transfusion |
| Cardiac marker analysers | Troponin at bedside in acute chest pain |
| Urine test strips (visual and readers) | UTI screening, proteinuria, glycosuria, ketonuria, haematuria |
| Glycated haemoglobin (HbA1c) analysers | Diabetes screening/monitoring in clinic |
| Whole blood glucose and lactate meters | DM monitoring, hypoglycaemia detection, sepsis (lactate) |
| Pregnancy tests | Urine hCG – ED, obstetrics, GP |
| Faecal occult blood | CRC screening |
| HIV testing | Rapid HIV antibody/antigen test in outreach settings |
| Drug-of-abuse testing | ED, occupational health, forensic |
5. Urine Dipstick Testing – Detailed Interpretation
The lecture devotes several slides to urine dipstick analysis. This is a revision topic but highly examinable because it tests understanding of the chemistry behind each pad.
Principle: Nitroprusside reaction-based methods. Detects Acetoacetate >> Acetone. β-Hydroxybutyrate is NOT measured. [1]
Why this matters clinically:
In diabetic ketoacidosis (DKA), the predominant ketone body is β-hydroxybutyrate (β-OHB), which can comprise up to 75% of total ketones. The urine dipstick uses the nitroprusside (sodium nitroferricyanide) reaction, which reacts with acetoacetate and (weakly) with acetone, but does NOT detect β-OHB at all.
Clinical implication:
- At presentation of severe DKA, the urine dipstick may paradoxically show only moderate ketones because most ketones are β-OHB.
- During treatment of DKA (with insulin and fluids), β-OHB is converted back to acetoacetate. The urine dipstick may then show increasing ketones even as the patient is improving — this is a well-known trap in clinical practice and exams.
- A serum/whole-blood β-OHB meter (also a POCT device) is superior for monitoring DKA.
High Yield – DKA Monitoring Trap
Do NOT use the urine ketone dipstick to monitor DKA treatment progress. The dipstick misses β-hydroxybutyrate and may show "worsening" ketones during successful treatment as β-OHB converts to acetoacetate. Use a blood β-OHB POCT meter instead.
The lecture references Patel et al. Pediatr Clin N Am 2006 for a table of false positives and negatives [1]
Key examples to know for exams:
| Dipstick Pad | False Positive | False Negative |
|---|---|---|
| Glucose | Strong oxidising agents (e.g., bleach contamination) | High ascorbic acid (vitamin C) intake |
| Protein (albumin) | Highly alkaline urine (pH > 8), concentrated urine, contamination with antiseptics (chlorhexidine) | Dilute urine, non-albumin proteins (Bence Jones protein / light chains in myeloma) |
| Blood / Haemoglobin | Myoglobin (rhabdomyolysis), semen, menstrual contamination, oxidising agents | High ascorbic acid, high specific gravity, captopril |
| Leukocyte esterase | Contamination, Trichomonas | Very high glucose, high specific gravity, high oxalic acid, ascorbic acid |
| Nitrite | Contamination with nitrite-containing substances, specimen standing too long at room temperature | Non-nitrate-reducing organisms (Enterococcus, Pseudomonas, S. saprophyticus), dilute urine, recent voiding (insufficient incubation time in bladder) |
| Ketones | Captopril, mesna, highly pigmented urine | β-OHB predominance (as in DKA) |
Ascorbic Acid (Vitamin C) – Universal Interferer
Ascorbic acid is a reducing agent that interferes with the oxidase-based chemistry of several dipstick pads (glucose, blood, nitrite, leukocyte esterase), causing false negatives. Patients taking high-dose vitamin C supplements are at risk.
6. Urine Pregnancy Test (hCG)
Lower limit of detection of urine hCG: 25 mIU/mL (varies in different test kits). Blood hCG concentrations: Non-pregnant < 5 IU/L. [1]
The test uses a lateral flow immunochromatographic assay (a "sandwich" immunoassay):
- Urine is applied to an absorbent pad.
- hCG in the urine binds to colloidal gold-conjugated anti-hCG antibody (mobile phase).
- The hCG–antibody complex migrates along the membrane and is captured by a second anti-hCG antibody immobilised at the test line → visible line appears.
- Excess conjugated antibody migrates further and is captured by an anti-mouse antibody at the control line → visible line confirms the test worked.
- One line (control only) = Negative
- Two lines (test + control) = Positive
- No lines = Invalid test (device malfunction, insufficient sample)
In pregnancy, hCG immunoreactivity is due to many variants: intact hCG, hCG-h (hyperglycosylated hCG), hCGn (nicked hCG), free β-hCG subunit [found in urine & serum], and hCGcf (core fragment of hCG) [urine only]. [1]
"Different POCT devices may recognise different variants" — "Negative does NOT mean patient is NOT pregnant." [1]
Why this is critical: Each POCT kit uses antibodies that may have different specificities for these hCG variants. A kit that only detects intact hCG may give a false negative in a patient whose predominant circulating form is free β-hCG or a degraded fragment.
From lecture slide [1]:
| Cause | Mechanism |
|---|---|
| Normal pregnancy | Trophoblast produces hCG |
| Abnormal pregnancy (ectopic, miscarriage) | Trophoblast tissue present but in abnormal location/state |
| Gestational trophoblastic disease (hydatidiform mole, choriocarcinoma) | Abnormal trophoblast proliferation → very high hCG |
| Germ cell tumours | Non-gestational tumours (e.g., testicular) producing hCG |
| Ectopic hCG-producing tumours (e.g., Ca lung) | Paraneoplastic hCG secretion |
| Pituitary hCG | Low-level hCG-like material from pituitary, especially post-menopause (shares α-subunit with LH/FSH/TSH) |
| Previous injection of hCG (athletes, bodybuilders) | Exogenous hCG for performance enhancement or infertility treatment |
| Immunoassay interferences | Heterophilic antibodies (e.g., HAMA) causing false-positive on lab assay |
| Cross-reactivity with LH | Unlikely with modern 2-site immunometric assays (historical issue) |
From lecture slide [1]:
| Cause of False Positive | Explanation |
|---|---|
| Biochemical pregnancy (early miscarriage) | hCG was truly elevated from a real conception that failed very early; technically not a "false" positive but clinically misleading |
| Missed reaction time / incorrect reading time | Reading the test too late allows non-specific migration → faint "positive" line |
| Drugs (e.g., hCG shot for infertility) | Exogenous hCG in the system |
| Evaporation lines | Urine drying on the strip leaves a faint colourless line misinterpreted as positive |
| Mislabelled specimens | Administrative error |
High Yield – Negative UPT ≠ Not Pregnant
A negative urine pregnancy test does NOT definitively exclude pregnancy. Reasons include: very early pregnancy (hCG below kit detection limit), dilute urine, device not detecting the relevant hCG variant. If clinical suspicion is high, send a serum quantitative β-hCG to the lab.
The lecture shows urine drug-of-abuse POCT devices [1]
These are also lateral flow immunoassay strips, but they work via a competitive inhibition format (opposite to pregnancy tests):
- No drug in urine → labelled antibody–drug conjugate binds to the test line → line appears = NEGATIVE
- Drug present in urine → drug in the sample competes with the conjugate → test line does NOT appear = POSITIVE (i.e., absence of a line is positive)
Important points:
- These are screening tests only. A positive result must be confirmed by a reference method (e.g., GC-MS or LC-MS/MS in the central lab).
- Cross-reactivity is common (e.g., pseudoephedrine causing false positive for amphetamines, poppy seeds for opiates).
- Chain of custody and specimen integrity are critical for medicolegal purposes.
8. Blood Glucose Meter (Glucometer)
"To determine the approximate blood glucose by a small drop of blood, pricking from skin by a lancet. The blood is placed on the test strip. For home monitoring of blood glucose in patients with diabetes mellitus and hypoglycaemia." [1]
The lecture lists three enzymatic methods [1]:
| Method | Enzyme | Cofactor | Key Point |
|---|---|---|---|
| Glucose Oxidase (GOx) | Glucose oxidase | O₂ | Specific for glucose; affected by oxygen tension (unreliable in hypoxia/hyperoxia) |
| GDH-PQQ | Glucose dehydrogenase | Pyrroloquinoline quinone | Non-selective for glucose – also detects maltose, xylose, galactose, icodextrin, immunoglobulins |
| GDH-FAD | Glucose dehydrogenase | Flavin adenine dinucleotide | More specific than GDH-PQQ |
| GDH-NAD | Glucose dehydrogenase | Nicotinamide adenine dinucleotide | Most specific GDH variant |
"GDH-PQQ is non-selective for glucose and it also detects other non-glucose sugars: maltose, xylose, galactose, icodextrin or immunoglobulins." — FDA Safety Alert, as cited in lecture [1]
Why is this dangerous?
- Patients on peritoneal dialysis use icodextrin-containing dialysate (e.g., Extraneal). Icodextrin is metabolised to maltose and maltotriose. A GDH-PQQ glucometer will falsely overestimate the blood glucose → the patient (or staff) may give insulin for a falsely high reading → fatal hypoglycaemia.
- Patients receiving intravenous immunoglobulin (IVIG) formulated with maltose face the same risk.
Critical Safety Point – GDH-PQQ and Icodextrin
Never use a GDH-PQQ-based glucometer in a patient on icodextrin peritoneal dialysis or receiving maltose-containing IVIG. The falsely elevated glucose reading may lead to inappropriate insulin administration and life-threatening hypoglycaemia. Use a glucose-oxidase or GDH-FAD/NAD device instead.
"Poor analytical accuracy at both low and high glucose levels. Usual dynamic range: 2.5 – 28 mmol/L. Dangerously low glucose levels ( < 2.0 mmol/L) could be missed." [1]
Why? Glucometers are designed for the ambulatory DM monitoring range (~4–20 mmol/L). At the extremes:
- Very low values ( < 2.0 mmol/L): The imprecision (coefficient of variation) of glucometers is typically ±15–20%. At 2.0 mmol/L, this means the true value could range from ~1.6 to 2.4 mmol/L — a critical difference. The meter might display "2.5" when the true glucose is 1.5 (neuroglycopaenic danger zone).
- Very high values ( > 28 mmol/L): The strip's enzyme reaction saturates; values plateau or give "HI" without a number.
"Always send a concomitant fluoride-oxalate blood sample to the main lab for verification." [1]
Why fluoride-oxalate? Fluoride inhibits glycolysis by enolase inhibition; oxalate chelates calcium and prevents clotting. Without fluoride, red cells continue to consume glucose in vitro at ~5–7% per hour → falsely low lab result.
"Take concomitant blood samples for Insulin, C-Peptide, Cortisol, GH, etc., if hypoglycaemia is clinically evident; but don't delay any clinical interventions to await the results – treat the hypoglycaemia straightaway after the blood sampling." [1]
Clinical reasoning: If a patient has genuine hypoglycaemia, you need to determine the cause (insulinoma, exogenous insulin, adrenal insufficiency, etc.). The diagnostic window closes the moment you give IV dextrose because insulin/C-peptide levels will change. So: draw the diagnostic bloods first, then treat immediately — don't wait for lab results before treating.
The slide mentions "Calibration" as a key point [1]
- Most modern glucometers self-calibrate via a code on the test strip container or a calibration chip.
- Whole blood vs. plasma calibration: Capillary blood glucometers measure whole blood glucose, but many are factory-calibrated to report plasma-equivalent values (roughly 11% higher than whole blood). This can cause confusion if compared directly to a central lab plasma glucose.
From the interferences lecture [3], additional factors affecting glucometer accuracy include:
- Haematocrit: High Hct (neonates, polycythaemia) → falsely low readings (less plasma per unit volume); low Hct (severe anaemia) → falsely high.
- Peripheral hypoperfusion/shock: Capillary blood does not reflect arterial glucose.
- Altitude, temperature, humidity: affect electrochemical reactions on test strips.
From the lecture slide [1]:
Specimen Handling Rules
| Rule | Rationale |
|---|---|
| Arterial blood specimen | Venous blood does not reflect oxygenation; arterial blood is the standard for acid-base and gas exchange assessment |
| Avoid air bubbles | Air bubbles equilibrate with blood → pO₂ rises artificially (~150 mmHg in room air), pCO₂ drops |
| Label specimen with GUM label | Patient identification and traceability |
| Refrigerate specimen if analysis is not done immediately | Metabolically active cells continue to consume O₂ and produce CO₂ and lactate at room temperature, altering results |
| Blood gas analysis must be performed within 90 minutes | Even refrigerated, prolonged storage causes significant drift in pO₂, pCO₂, pH, and lactate |
Pre-analytical Errors – The Biggest Threat to ABG Accuracy
Most errors in blood gas results are pre-analytical: air bubbles, delayed analysis, wrong patient label, venous instead of arterial, insufficient sample volume, and clotted specimens. These are all avoidable with proper training – which is why the lecture emphasises SOP, training, and certification.
10. Other POCT Applications (Brief Notes)
- Rapid troponin POCT in chest pain assessment in ED.
- Useful in resource-limited settings or where central lab TAT exceeds 60 minutes.
- Sensitivity may be lower than high-sensitivity lab troponin assays.
- Activated Clotting Time (ACT): used in cardiac catheterisation lab and cardiac surgery to monitor heparin effect.
- Thromboelastography (TEG) / ROTEM: used in massive transfusion protocols, liver transplant, obstetric haemorrhage.
- Enables same-visit DM management in primary care.
- Must be NGSP-certified and traceable to DCCT reference.
- Guaiac-based (older) vs. faecal immunochemical test (FIT, newer and more specific for lower GI bleeding).
- 4th generation: detects both HIV-1/2 antibodies and p24 antigen.
- Reduces window period compared to antibody-only tests.
- A positive rapid test must be confirmed by lab-based Western blot or supplementary antibody differentiation assay.
| Feature | POCT | Central Lab |
|---|---|---|
| TAT | Minutes | Hours (may be 30 min to several hours) |
| Sample volume | Very small (capillary) | Larger (venous) |
| Operator | Nurse, doctor, patient | Laboratory scientist |
| Accuracy | Good but generally inferior at extremes | Gold standard |
| Precision (CV%) | Higher CV (less precise) | Lower CV (more precise) |
| Menu | Limited (single analyte or small panel) | Comprehensive |
| QC/QA | Required but often less rigorously implemented | Stringent, continuous |
| Cost per test | Higher (reagent cartridges) | Lower (economies of scale) |
| Connectivity | May not auto-upload to EMR | Fully integrated with LIS/EMR |
| Best suited for | Time-critical decisions, remote settings | Definitive diagnosis, monitoring, complex panels |
| Topic | Relevant GC/CFB Lecture | Connection |
|---|---|---|
| Laboratory test interpretation | CFB MED10 (Use of Laboratory Test) [2] | POCT as one modality; understanding sensitivity/specificity applies equally |
| Interferences | Chemical Pathology Seminar on Interferences [3] | Haematocrit, drugs, oxygen tension affecting glucometers |
| DKA monitoring | GC 157 (Paediatric Chemical Pathology) | β-OHB meters superior to urine ketone dipstick |
| Infection diagnosis | GC 101 (Diagnosis of Infections) | RADT, rapid lateral-flow assays for HIV, COVID-19, TB urine LAM |
| Pregnancy | CFB OGPAE01-1 | Urine/serum hCG in early pregnancy |
| Pharmacogenomics | Intro to Clinical Pharmacology (I) [6] | VerifyNow assay (POCT for platelet function) to detect clopidogrel resistance |
Exam Intelligence
| Trap | How to Avoid |
|---|---|
| "Urine dipstick ketones are negative, so no DKA" | Remember dipstick misses β-OHB, the predominant ketone in DKA |
| "Negative urine pregnancy test excludes pregnancy" | No – can be falsely negative due to dilute urine, early pregnancy, variant-specific antibodies |
| "Glucometer reading of 2.5 mmol/L is accurate" | Glucometers have poor accuracy at extremes; always confirm with lab fluoride-oxalate sample |
| "GDH-PQQ glucometer is interchangeable with GOx" | GDH-PQQ detects maltose/icodextrin → dangerous in PD patients |
| "POCT doesn't need QC because it's just bedside" | POCT requires IQC and EQA just like central lab |
| "A faint line on pregnancy test = negative" | A faint line is positive; only NO line is negative |
| "Wait for lab confirmation before treating hypoglycaemia" | Treat immediately after drawing diagnostic samples; never delay |
- Specificity vs Sensitivity of RADT: Specificity is > 95% (excellent at ruling IN GAS); sensitivity is 70-90% (not great at ruling OUT → confirm negatives with culture in children).
- Fluoride-oxalate tube: This is the correct tube for a glucose sample sent to the lab because fluoride inhibits glycolysis. A plain tube or EDTA tube will give falsely low glucose due to ongoing glycolysis.
- GDH-PQQ vs GOx: GDH-PQQ is non-specific (cross-reacts with maltose, icodextrin); GOx is specific for glucose but affected by oxygen tension.
Based on a thorough review of the indexed past papers, the following question is relevant to this lecture:
2025 Fourth Summative MCQ Q6 [7]:
"Disease diagnosis often requires ancillary investigations such as laboratory testing. A laboratory test for detecting a rare inherited metabolic disorder has a very high specificity but moderate sensitivity. Which of the following clinical scenarios BEST suits this test?"
- A. Confirmatory testing after a positive screening test.
- B. Initial screening for asymptomatic population.
- C. Population-wide epidemiological studies.
- D. Testing in emergency setting for rapid diagnosis.
Answer: A. Rationale: A test with very high specificity is excellent for ruling IN disease (few false positives) and is therefore best used as a confirmatory test. A screening test needs high sensitivity (to catch all cases, even at the cost of some false positives). This concept directly applies to POCT – e.g., a positive RADT (high specificity) confirms GAS pharyngitis, but a negative result (moderate sensitivity) needs culture confirmation.
No other past paper questions directly examining POCT content (urine dipstick interpretation, glucometer interferences, hCG variants, blood gas specimen handling) were identified in the indexed past papers. However, POCT principles underpin many clinical scenarios tested in minicases and SAQs (e.g., interpreting a glucometer reading in a DKA case, or managing hypoglycaemia).
High Yield Summary
POCT = Any test at bedside enabling immediate clinical action → key benefit is reduced TAT but ONLY if results are accurate and reliable.
Governance: SOP, Training/Certification, IQC, EQA, Documentation, Maintenance, Safety – all mandatory.
Urine dipstick ketones: Nitroprusside method detects acetoacetate/acetone but NOT β-OHB (the predominant ketone in DKA) → use blood β-OHB meter for DKA monitoring.
Urine pregnancy test: Threshold ~25 mIU/mL; different kits detect different hCG variants → negative does NOT exclude pregnancy; causes of elevated hCG include ectopic, GTD, germ cell tumours, pituitary hCG, exogenous injection, immunoassay interference.
Glucometer: GOx (specific, affected by O₂), GDH-PQQ (non-specific – detects maltose/icodextrin → NEVER use in PD patients), GDH-FAD/NAD (more specific). Dynamic range ~2.5–28 mmol/L; poor accuracy at extremes. Always send fluoride-oxalate confirmatory sample. In hypoglycaemia: draw insulin/C-peptide/cortisol/GH first, then treat immediately.
ABG POCT: Arterial specimen, no air bubbles, analyse within 90 min, refrigerate if delayed.
Drug of abuse POCT: Screening only → confirm positives with GC-MS/LC-MS/MS. Competitive immunoassay (absence of line = positive).
Active Recall - POCT Lecture Notes
[1] Lecture slides: GC 158. Point-of-care testing (POCT).pdf [2] Lecture slides: CFB (MED10) The use of laboratory test in clinical medicine.pdf (p.45-46) [3] Lecture slides: Chemical Pathology Seminar_Interferences in laboratory testing 20240912.pdf [4] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p.131) [5] Senior notes: Ryan Ho Respiratory.pdf (p.51) [6] Senior notes: Introduction to Clinical pharmacology (I) (Pharmaco- Genomics, Precision Medicine).pdf (p.3) [7] Past papers: 2025 Fourth Summative MCQ.pdf (Q6, p.4)
GC157 Paediatric Chemical Pathology
Paediatric chemical pathology is the subspecialty of clinical biochemistry focused on the diagnosis and monitoring of metabolic, endocrine, and biochemical disorders in neonates, infants, and children.
GC159 Research Ethics (notes)
Research ethics is the framework of principles and regulatory guidelines—including informed consent, beneficence, non-maleficence, justice, and institutional review—that govern the conduct of biomedical and clinical research involving human subjects.