Physical And Chemical Urinalysis

Physical Examination: Color, Clarity, And Specific Gravity

Routine urinalysis opens with the physical exam. Normal color is pale yellow to amber from urochrome pigment. The ASCP BOC favors color-cause pairings: red/pink = blood, hemoglobin, beets, or rifampin; dark yellow-brown with yellow foam = bilirubin; red-brown that darkens on standing = porphyrins or homogentisic acid (alkaptonuria); black on standing = melanin. Clarity terms run clear, hazy, cloudy, turbid. Common turbidity causes: amorphous urates (clear on warming), amorphous phosphates and carbonates (clear with dilute acetic acid), WBCs, bacteria, and squamous epithelial cells.

Specific gravity (SG) measures dissolved solute density. Normal random urine is 1.003-1.035; most well-hydrated specimens fall 1.010-1.025. Memorize these patterns:

Refractometry is the routine SG method, reading 1.000-1.035 by refractive index; it must be temperature-compensated and zeroed with distilled water (1.000). The reagent-strip SG pad measures ionic concentration only via a polyelectrolyte pKa shift, so it misses non-ionic solutes (glucose, contrast media). High pH (>6.5) falsely lowers the strip SG, requiring a manufacturer-specified 0.005 correction. Glucose adds roughly 0.003-0.004 to refractometer SG per g/dL, and protein adds about 0.003 per g/dL; correct large urine SG values before reporting.

Chemical Examination: Reagent-Strip Reactions And Interferences

Each reagent strip pad is a distinct chemistry. The exam loves false-positive/false-negative scenarios, so learn the mechanism, not just the number.

• pH (double indicator, methyl red + bromthymol blue): range 5.0-9.0. A pH >8 on a non-fresh specimen usually means old urine with urea-splitting bacteria (Proteus), not true alkalosis.
• Protein (protein-error-of-indicators dye, tetrabromphenol blue): most sensitive to albumin; misses Bence Jones light chains. Highly buffered alkaline urine gives a false positive. Confirmatory sulfosalicylic acid (SSA) precipitates all proteins, so SSA-positive with a negative pad suggests globulins or light chains.
• Glucose (glucose oxidase/peroxidase): specific for glucose; false negatives from high ascorbic acid and ketones, false positives from oxidizing detergents (bleach). Renal threshold ~180 mg/dL.
• Ketones (sodium nitroprusside): reacts strongly with acetoacetate, weakly with acetone, and NOT with beta-hydroxybutyrate, the dominant DKA ketone, so an early DKA strip can underread.
• Blood (pseudoperoxidase): reacts to RBCs, free hemoglobin, AND myoglobin. Speckled pattern = intact RBCs (hematuria); uniform = hemoglobinuria or myoglobinuria. Pink plasma points to hemoglobinemia; clear plasma with positive blood and muscle injury points to myoglobin.
• Bilirubin (diazo): conjugated bilirubin only; light- and ascorbic-acid-sensitive.
• Urobilinogen (Ehrlich or diazo): normal is a trace; absence is NOT reportable by strip.
• Nitrite (Greiss): requires gram-negative nitrate reducers plus 4+ hours bladder incubation. A negative nitrite never excludes UTI.
• Leukocyte esterase: detects granulocyte esterase even after WBC lysis; false negatives from high glucose, protein, or ascorbic acid.

Web-verified anchors: the MLS(ASCP) exam is 100 multiple-choice items in 2.5 hours, computer-adaptive, scaled 100-999 with 400 passing. Ascorbic acid >40 mg/dL is the single most tested reagent-strip interferent.

High-Yield Correlations And Common Traps

The ASCP BOC rarely asks you to merely recall a normal value; it asks you to correlate a physical, chemical, and microscopic triad and pick the single best interpretation. Build the habit of reading all three before answering.

Consider the classic diabetic-ketoacidosis pattern: dark amber urine, high specific gravity (often >1.030 from glucose), strongly positive glucose, and positive ketones. Remember the ketone trap — the nitroprusside pad detects acetoacetate and acetone but not beta-hydroxybutyrate, which is the dominant ketone early in severe DKA. A patient deep in acidosis can therefore show only a moderate ketone reading; the result underrepresents true ketosis until therapy converts beta-hydroxybutyrate back to acetoacetate, paradoxically raising the urine ketone as the patient improves.

A second high-yield pairing is the urobilinogen-versus-bilirubin liver workup:

Bilirubin appears in urine only when it is conjugated (water soluble), so a positive urine bilirubin always signals hepatobiliary disease, never hemolysis alone. Increased urobilinogen with negative bilirubin points to hemolysis.

Finally, watch the foam test as a quick bench clue: white foam that does not dissipate suggests proteinuria, while yellow foam that persists suggests bilirubinuria from the surfactant-like bile pigments. Color traps appear constantly: phenazopyridine (Pyridium) turns urine orange and masks pads; rifampin and beets produce red-orange; and homogentisic acid (alkaptonuria) and melanin darken urine only on standing. Train yourself to flag any chemical-microscopic discrepancy as the seed of a one-best-answer question rather than reporting it uncritically.