ABPath Clinical Pathology cheat sheet

Anion gap = (Na+) − (Cl− + HCO3−); reference ~8–12 mmol/L; add K+ only if the lab's formula specifies it.

Corrected calcium (mg/dL) = measured Ca + 0.8 × (4.0 − albumin g/dL); ionized calcium is unaffected by albumin.

Serum osmolality (mOsm/kg) ≈ 2[Na+] + glucose/18 + BUN/2.8; osmolal gap >10 suggests unmeasured osmoles (methanol, ethylene glycol, isopropanol).

Friedewald LDL = TC − HDL − TG/5 (mg/dL), valid only when TG <400 mg/dL; use direct or Martin-Hopkins method above that.

High anion gap acidosis mnemonics: ketoacidosis, lactic acidosis, renal failure, toxins (salicylate, methanol, ethylene glycol, propylene glycol).

Non-anion gap acidosis: GI bicarbonate loss, renal tubular acidosis, carbonic anhydrase inhibitors, large-volume normal saline; check urine anion gap.

Troponin (cTnI/cTnT) is the preferred necrosis marker; a rise-and-fall pattern with at least one value above the 99th percentile URL defines acute myocardial injury.

HbA1c reflects ~2–3 months of glycemia; unreliable with hemoglobin variants, recent transfusion, hemolysis, or altered red cell survival.

CK-MB, myoglobin, and LDH are no longer first-line for ACS; LDH-1/LDH-2 flip is a classic but nonspecific marker of hemolysis or MI.

MCV = (Hct ÷ RBC count) × 10 (fL); MCH = Hb ÷ RBC; MCHC = Hb ÷ Hct; use them to classify anemia as microcytic, normocytic, or macrocytic.

Reticulocyte index = retic % × (patient Hct ÷ normal Hct) ÷ maturation correction (~2 for Hct 25–35%); an elevated corrected retic indicates a regenerative response.

Iron deficiency: low ferritin, low serum iron, high TIBC, low transferrin saturation; anemia of chronic disease: low iron and TIBC, normal-to-high ferritin.

Lead poisoning and sideroblastic anemia show ring sideroblasts and often basophilic stippling; thalassemia shows target cells and normal or high iron stores.

Intrinsic pathway: factors VIII, IX, XI, XII; extrinsic: VII; common: I, II, V, X. PT screens extrinsic/common, aPTT screens intrinsic/common.

Mixing study: correction of a prolonged PT/aPTT with normal plasma suggests factor deficiency; failure to correct suggests an inhibitor (e.g., lupus anticoagulant, factor VIII inhibitor).

DIC: prolonged PT/aPTT, low fibrinogen, elevated D-dimer/fibrin degradation products, schistocytes, and thrombocytopenia.

CML: t(9;22) BCR-ABL1; basophilia and left shift are typical. APL: t(15;17) PML-RARA with DIC risk and Auer rods.

Flow cytometry: CD34/CD117 for blasts, CD13/CD33 for myeloid, CD19/CD20/CD22 for B cells, CD3/CD4/CD8 for T cells, CD41/CD61 for megakaryocytic lineage.

Gram-positive cocci in clusters = Staphylococcus; in chains = Streptococcus; in pairs = Streptococcus pneumoniae or Enterococcus.

Catalase-positive, coagulase-positive Gram-positive cocci = Staphylococcus aureus; coagulase-negative = other staphylococci.

Optochin-sensitive, bile-soluble alpha-hemolytic streptococci = S. pneumoniae; optochin-resistant = viridans streptococci.

Lancefield grouping: group A = S. pyogenes (bacitracin-sensitive), group B = S. agalactiae (hippurate-positive, CAMP-positive).

Lactose-fermenting Gram-negative rods on MacConkey appear pink; non-lactose fermenters are colorless (e.g., Pseudomonas, Salmonella, Shigella).

Oxidase-positive Gram-negative rods include Pseudomonas, Neisseria, Vibrio, and Aeromonas; Enterobacterales are oxidase-negative.

MRSA detection uses cefoxitin disk or mecA/PBP2a testing; ESBL screen uses ceftazidime/cefotaxime ± clavulanate; carbapenemase testing is required for CRE.

Blood culture contamination: coagulase-negative staphylococci, diphtheroids, and viridans streptococci in a single bottle often reflect skin flora; S. aureus and Gram-negative rods are almost always pathogens.

Mycobacterium tuberculosis: acid-fast, slow-growing, niacin- and nitrate-positive; use liquid culture and nucleic acid amplification for rapid detection.

ABO compatibility: type O has anti-A and anti-B; type AB has neither; type A has anti-B; type B has anti-A.

Rh(D) negative patients should receive Rh(D)-negative red cells; anti-D can cause hemolytic disease of the newborn and delayed hemolytic transfusion reactions.

Antibody screen: indirect antiglobulin test (IAT) detects unexpected antibodies; a positive screen requires identification and antigen-negative units.

Immediate spin crossmatch detects ABO incompatibility; full crossmatch includes IAT and is required for patients with known alloantibodies.

Delayed hemolytic transfusion reaction: fall in hemoglobin, positive DAT, and new alloantibody appearing 3–14 days after transfusion.

Direct antiglobulin test (DAT) detects antibody or complement on red cells; a positive DAT occurs in autoimmune hemolysis, HDFN, and drug-induced hemolysis.

Anaphylaxis, TRALI, and acute hemolytic reactions are the most severe transfusion reactions; febrile non-hemolytic and urticarial reactions are the most common.

Antinuclear antibodies (ANA) are sensitive but not specific for SLE; anti-dsDNA and anti-Sm are more specific, and complement C3/C4 are often low in active lupus.

ANCA: c-ANCA (anti-proteinase 3) is associated with granulomatosis with polyangiitis; p-ANCA (anti-myeloperoxidase) with microscopic polyangiitis.

Karyotype resolution is ~5–10 Mb; FISH detects specific loci (~100–200 kb); chromosomal microarray detects copy-number changes at kilobase resolution but not balanced rearrangements.

Translocation nomenclature: t(9;22)(q34;q11.2) means breakpoints on chromosome 9 band q34 and chromosome 22 band q11.2.

Common translocations: t(8;21) RUNX1-RUNX1T1 (AML), t(15;17) PML-RARA (APL), t(9;22) BCR-ABL1 (CML/ALL), t(14;18) IGH-BCL2 (follicular lymphoma).

BCR-ABL1 quantitative PCR monitors CML response; major molecular response is BCR-ABL1 ≤0.1% on the international scale.

JAK2 V617F is present in most polycythemia vera and about half of essential thrombocythemia and primary myelofibrosis; CALR and MPL mutations occur in JAK2-negative cases.

EGFR, ALK, ROS1, and KRAS testing guide lung cancer therapy; BRAF V600E testing guides melanoma and hairy cell leukemia therapy.

BRCA1/BRCA2 germline mutations increase breast and ovarian cancer risk; tumor testing for HRD can guide PARP inhibitor use.

FISH for HER2 amplification uses a HER2/CEP17 ratio; ratio ≥2.0 or average HER2 copy number ≥6 signals per cell indicates amplification.

Next-generation sequencing identifies variants but requires orthogonal confirmation for clinically actionable findings; variant interpretation uses ACMG/AMP criteria.

Analytic sensitivity = TP/(TP+FN); specificity = TN/(TN+FP); positive predictive value depends on prevalence and equals TP/(TP+FP).

Coefficient of variation (CV) = (SD ÷ mean) × 100%; CV is used to compare precision across assays with different units.

Six Sigma = (TEa − |bias|) ÷ CV; higher values indicate fewer defects; ≥6 is world-class, <3 is unacceptable.

Westgard rules: 1-3s rejects a single result >3 SD; 2-2s rejects two consecutive results >2 SD on the same side; R-4s rejects a range >4 SD between two levels; 4-1s rejects four consecutive >1 SD on one side.

Levey-Jennings charts display QC results over time; shifts indicate sudden bias, trends indicate gradual drift, and increased scatter indicates imprecision.

CLIA requires proficiency testing, biannual calibration verification, and documented competency assessment; waived tests are exempt from most CLIA QC but not from manufacturer instructions.

Critical value reporting requires documented read-back and time of notification; the laboratory must define critical limits for each analyte.

Turnaround time (TAT) is measured from order or receipt to result reporting; monitor median and 90th percentile rather than mean alone.

LOINC codes identify laboratory tests and observations; SNOMED CT codes clinical findings; HL7 interfaces exchange orders and results between LIS and EHR.