Free ASCP MLS Exam Practice Questions Mock Test: Part 10 – Urinalysis (Physical)

• Urine clarity should be assessed immediately after gentle but thorough agitation of the sample to evenly suspend any particles (e.g., cells, crystals, mucus) that may have settled. This ensures an accurate visual evaluation of turbidity.

• Clarity is typically graded as:

  • Clear (no visible particles).

  • Hazy (slight cloudiness).

  • Cloudy (obscured visibility, suggests WBCs, bacteria, or crystals).

  • Turbid (dense, milky appearance, e.g., pyuria or chyluria).

Why Not the Others?

• a) Centrifugation: Alters clarity by pelleting sediment; clarity is assessed before centrifugation.

• c) Adding sulfosalicylic acid: Used to confirm proteinuria (causes precipitation), not clarity.

• d) Warming to 37°C: May dissolve amorphous urates/crystals but is not routine for clarity assessment.

Key Points:

• False cloudiness:

  • Refrigeration can precipitate crystals (e.g., phosphates).

  • Non-pathologic mucus may cause mild haze.

• Clinical relevance: Cloudy urine + dysuria = UTI suspicion.

• Crystals (e.g., phosphates, urates) are a common cause of cloudiness in urine that appears or worsens after refrigeration. These crystals form when the urine cools, especially if it was initially alkaline (phosphates) or highly concentrated (urates).

• This type of cloudiness is typically benign and resolves when the sample is warmed.

Why Not the Others?

• a) WBCs – White blood cells (indicating infection) cause cloudiness immediately, not just after refrigeration.

• c) Bacteria – Bacterial growth can cause cloudiness, but this usually develops over time at room temperature, not specifically from chilling.

• d) Yeast – May cause turbidity, but this is unrelated to refrigeration and is often seen as small white clumps.

Melanin, or its precursor metanephrine, can cause urine to appear brown or black upon standing, especially in acidic urine. This is due to oxidation of the pigment when exposed to air. It can be a sign of melanoma.

hy Not the Others?

• a) Urobilinogen oxidizes into urobilin when urine is exposed to air over time, turning urine darker yellow or brown.

• b) Myoglobin: Causes reddish-brown urine when fresh (does not darken further with standing).

• d) Light exposure to bilirubin: Degrades bilirubin to greenish biliverdin, not brown/black.

Urea contributes the most to high urine specific gravity under normal physiological conditions, as it is the primary nitrogenous waste product excreted by the kidneys and is present in significant amounts.

However, in pathological conditions like diabetes mellitus, glucose can also significantly raise specific gravity. But under normal conditions, urea is the major contributor.

Why Not the Others?

• a) Protein: Contributes minimally (1 g/dL protein raises SG by only ~0.003).

• b) Glucose: Significant in diabetes (1 g/dL glucose raises SG by ~0.004), but less than electrolytes in most cases.

• d) Sodium (Na⁺) and its associated anions (e.g., Cl⁻) are the primary contributors to high urine specific gravity (SG)

• Myoglobinuria (e.g., from rhabdomyolysis) releases CK from damaged muscle, causing elevated serum CK levels (often >5,000 U/L).

• Hemoglobinuria (e.g., hemolysis) does not raise CK but may show low serum haptoglobin and LDH elevation.

Why Not the Others?

• a) Microscopic examination: Both myoglobin and hemoglobin cause dipstick-positive urine with no RBCs (unlike hematuria).

• b) Reagent strip for blood: Cannot differentiate hemoglobin vs. myoglobin (both test positive).

• d) Specific gravity: Nonspecific; both conditions may increase SG.

• Colorless urine typically occurs due to overhydration, where excessive water intake dilutes the urine, reducing the concentration of urochrome (the pigment responsible for yellow color).

• This is a physiologic response and not a sign of disease.

Why Not the Others?

• a) After strenuous exercise: Urine may be darker (concentrated due to fluid loss via sweat).

• b) In the early morning: Urine is usually dark yellow (most concentrated after overnight fasting).

• d) Due to proteinuria: Causes foamy urine, not color changes.

Key Points:

• Pathologic colorless urine: Rarely, diabetes insipidus (extreme polyuria) or chronic kidney disease (isosthenuria).

• Clinical correlation: Correlate with specific gravity (low in overhydration).

• Red blood cells (RBCs) in urine (hematuria) typically give it a pink, red, or cola-colored hue, depending on concentration and pH.

  • Fresh RBCs: Bright red/pink (common in lower UTIs or trauma).

  • Acidic urine + time: RBCs lyse, releasing hemoglobin, which turns brownish (e.g., glomerular bleeding).

Why Not the Others?

• a) Milky appearance: Caused by pyuria (WBCs), chyle, or crystals—not RBCs.

• c) Brown color: Seen with hemoglobinuria/myoglobinuria or oxidized RBCs (older hematuria).

• d) Green hue: Suggests Pseudomonas infection or medications (e.g., propofol), not hematuria.

Key Points:

• Dipstick positive for blood + RBCs on microscopy = True hematuria.

• No RBCs but dipstick positive? Suspect hemoglobinuria/myoglobinuria.

• Polyuria is defined as excessive urine output (>3,000 mL/day in adults or >2.5 L/m²/day in children). It results from:

  • Water diuresis: Diabetes insipidus (ADH deficiency/resistance).

  • Osmotic diuresis: Uncontrolled diabetes mellitus (glucose excretion).

  • Psychogenic polydipsia: Excessive fluid intake.

Why Not the Others?

• a) Anuria: <100 mL/day (e.g., renal failure, obstruction).

• b) Oliguria: <400 mL/day (e.g., dehydration, acute kidney injury).

• c) Nocturia: Frequent urination at night, regardless of total volume.

Key Points:

• Diagnostic approach:

  • 24-hour urine collection confirms volume.

  • Urine osmolality/specific gravity: Distinguishes water vs. osmotic diuresis.

• Clinical urgency: Polyuria with hypernatremia suggests diabetes insipidus.

• After radiocontrast administration, urine osmolality (measured by osmometry) is the gold standard for assessing concentration because:

  • Radiocontrast dyes (e.g., iohexol) are non-ionic but osmotically active, artificially elevating specific gravity (SG) via refractometry or dipsticks.

  • Osmometry directly measures total solute particles/kg water, unaffected by solute type, providing an accurate concentration assessment .

Why Not the Others?

• b) Refractometry: Overestimates SG due to high refractive index of contrast dyes (e.g., SG may read >1.040) .

• c) Spectrophotometry: Used for bilirubin/urobilinogen, not concentration.

• d) Densitometry: Rare in clinical labs; also skewed by radiocontrast .

Key Points:

• Clinical context:

  • Post-contrast AKI monitoring: Osmolality confirms true renal concentrating ability.

  • Hydration status: Contrast dyes can mimic dehydration via SG artifacts.

• Alternative: Urine osmolal gap (measured vs. calculated osmolality) detects exogenous solutes .

• Foul-smelling urine is most commonly caused by bacterial infection (e.g., E. coli, Proteus). These bacteria break down urea into ammonia, producing a strong, unpleasant odor.

• Proteus infections are particularly notorious for a pungent smell due to ammonia production and struvite stone formation.

Why Not the Others?

• a) Ketones: Give urine a fruity/sweet odor (e.g., diabetic ketoacidosis).

• b) Glucosuria: Typically odorless unless secondary infection occurs.

• d) Proteinuria: No distinct smell unless complicated by infection.

• Caramel-scented urine in neonates is a hallmark symptom of maple syrup urine disease (MSUD), a rare genetic disorder caused by the inability to metabolize branched-chain amino acids (leucine, isoleucine, and valine). The urine (and often sweat/earwax) emits a distinctive sweet, maple syrup-like odor, resembling caramel or burnt sugar .

• Onset: Symptoms typically appear within 48 hours to 1 week after birth, with the odor becoming noticeable as protein metabolism accelerates .

Why Not the Others?

• a) Cystinuria: Causes recurrent kidney stones but no odor change in urine .

• b) Alkaptonuria: Leads to black urine upon standing (due to homogentisic acid oxidation), not a sweet smell .

• c) Phenylketonuria (PKU): Produces a musty/mousy odor from phenylalanine metabolites, not caramel-like .

Key Points:

• Diagnosis:

  • Newborn screening (blood tests for elevated branched-chain amino acids) .

  • Urine amino acid analysis confirms the diagnosis .

• Urgency: Untreated MSUD can cause metabolic crises, seizures, coma, and death

• Reagent strip specific gravity (SG) measures ionic concentration (primarily Na⁺, K⁺, Cl⁻) via a polyelectrolyte system that releases hydrogen ions in proportion to urine cations. This alters the pH of a pH-sensitive dye (e.g., bromothymol blue), causing a color change correlated with SG .

• Limitation: Strips do not detect non-ionic solutes (e.g., glucose, urea), potentially underestimating true SG in glycosuria/proteinuria .

Why Not the Others?

• a) Color/clarity: Visual properties are unrelated to the strip’s SG reaction .

• c) Total volume: Irrelevant; SG is a ratio independent of volume .

• d) Cellular content: RBCs/WBCs do not affect the ionic pad (though hemolysis may release ions) .

Key Points:

• Refractometers are more accurate for SG as they measure all solutes (not just ions).

• Clinical tip: Compare strip SG with refractometer results if discrepancies arise (e.g., in diabetes).

• Urine with a specific gravity (SG) of 1.003 is extremely dilute, indicating high water content and low solute concentration. This results in a colorless or very pale yellow appearance, as the pigment urochrome is significantly diluted.

• Common causes include:

  • Excessive fluid intake (e.g., psychogenic polydipsia).

  • Diabetes insipidus (ADH deficiency or resistance).

  • Diuretic use.

Why Not the Others?

• a) Amber / d) Dark yellow: Seen with concentrated urine (SG >1.020, e.g., dehydration).

• b) Yellow: Typical of normal urine (SG 1.005–1.030).

Key Points:

• Clinical correlation:

  • Polyuria + colorless urine: Suggests diabetes insipidus or water overload.

  • SG 1.003 + hyponatremia: May indicate SIADH (dilute urine despite low serum osmolality).

• Dipstick confirmation: Low SG + negative glucose/ketones.

• A specific gravity (SG) of 1.040 is abnormally high and typically suggests interference from radiopaque contrast media (e.g., IV iodinated dyes used in CT scans). These agents are non-ionic but dramatically increase urine density, causing a falsely elevated SG via refractometry.

• Other possible (but less likely) causes:

  • Extreme dehydration (SG rarely exceeds 1.035 naturally).

  • Massive glycosuria/proteinuria (would require unrealistic concentrations, e.g., >5 g/dL glucose).

Why Not the Others?

• a) Normal hydration: SG should be 1.005–1.030; 1.040 is pathologic or artifactual.

• b) Accurate result: While technically “accurate” for total solutes, 1.040 is non-physiologic without exogenous substances.

• d) Proteinuria: Even nephrotic-range proteinuria (e.g., 3.5 g/day) rarely elevates SG beyond 1.035.

• Bilirubin is highly light-sensitive and rapidly degrades when exposed to UV light (e.g., sunlight or fluorescent lamps). This can lead to false-negative results if urine is not tested promptly or stored in opaque containers.

• Breakdown product: Bilirubin oxidizes into biliverdin, turning urine greenish and masking its original yellow-brown color.

Why Not the Others?

• a) Protein: Stable in light; no significant degradation.

• c) Nitrite: Affected by bacterial overgrowth (not light).

• d) Ketone: Acetone evaporates at room temperature, but light exposure has minimal impact.

Key Points:

• Specimen handling:

  • Test bilirubin immediately or shield urine from light (e.g., use amber tubes).

  • Refrigeration slows degradation but doesn’t replace light protection.

• Clinical impact: Missed bilirubinuria can delay diagnosis of hepatobiliary disease.

• In hepatic or obstructive liver disease, conjugated bilirubin (water-soluble) is excreted into the urine, giving it a dark amber or brown color (bilirubinuria). This occurs due to:

  • Biliary obstruction (e.g., gallstones, tumors).

  • Hepatocellular damage (e.g., hepatitis, cirrhosis).

• The urine may also appear foamy due to bilirubin’s surfactant properties.

Why Not the Others?

• a) Biliverdin: A green oxidative product of bilirubin, seen in old bile but not typically in urine.

• c) Phenazopyridine: Causes orange urine (a medication effect, unrelated to liver disease).

• d) Melanin: Produces black urine (e.g., metastatic melanoma), not amber/brown.

Key Points:

• Dipstick confirmation: Positive for bilirubin (diazo reaction).

• Clinical correlation:

  • Jaundice, clay-colored stools (lack of stercobilin).

  • Elevated serum direct (conjugated) bilirubin.

• Isosthenuria refers to the inability of the kidneys to concentrate or dilute urine, resulting in a fixed specific gravity (SG) of ~1.010 (the same as plasma ultrafiltrate). This occurs because:

  • The renal tubules lose their ability to reabsorb water/solutes (e.g., in chronic kidney disease or acute tubular necrosis).

  • The kidneys produce urine that is isosmotic to plasma, regardless of hydration status.

Why Not the Others?

• a) Glomerulonephritis: Typically causes hematuria/proteinuria, not fixed SG.

• b) Pyelonephritis: May cause WBCs/bacteria in urine but does not fix SG.

• d) Dehydration: Leads to high SG (>1.030), not 1.010.

• Arginine vasopressin (AVP) deficiency, also called central diabetes insipidus (DI), leads to hyposthenuria (urine specific gravity <1.005). This occurs because:

  • AVP (antidiuretic hormone) is required for water reabsorption in the renal collecting ducts.

  • Without AVP, the kidneys excrete large volumes of dilute urine, regardless of hydration status.

Why Not the Others?

• a) Glycosuria: Caused by hyperglycemia (e.g., diabetes mellitus), not AVP deficiency.

• b) Proteinuria: Results from glomerular damage (e.g., nephrotic syndrome).

• d) Bilirubinuria: Indicates hepatobiliary disease (e.g., conjugated hyperbilirubinemia).

Key Points:

• Diagnosis:

  • Water deprivation test: Confirms inability to concentrate urine.

  • Response to desmopressin (DDAVP): Distinguishes central DI (improves) from nephrogenic DI (no response).

• Clinical triad: Polyuria, polydipsia, hyposthenuria.

• Prolonged room temperature storage of urine leads to bacterial multiplication (especially if initially contaminated) and breakdown of urea into ammonia by urease-producing bacteria (e.g., Proteus). This causes:

  • Increased turbidity: Due to bacterial growth and precipitation of solutes (e.g., phosphates) .

  • Foul odor: From ammonia production .

  • False-positive nitrites: Bacterial metabolism of nitrates .

Why Not the Others?

• a) Increase in bilirubin: Bilirubin degrades into biliverdin upon light exposure (not storage time) .

• b) Decrease in specific gravity: SG remains stable unless evaporation concentrates the sample (rare) .

• d) Increased clarity: Only occurs if crystals dissolve (unlikely; turbidity usually worsens) .

Key Points:

• Artifacts of delayed testing:

  • False microscopy results: RBCs/WBCs lyse, casts degrade .

  • pH rise: Due to urea breakdown .

• Solution: Refrigerate samples if testing is delayed >2 hours .

• Physical characteristics of urine are observable properties assessed visually or by simple tests. These include:

  • Color (e.g., yellow, red, brown).

  • Clarity (clear, hazy, cloudy).

  • Odor.

  • Specific gravity (density).

Why Not the Others?

• a) Nitrites, b) Leukocyte esterase, and d) Urobilinogen are chemical properties detected by dipstick testing, not direct observation.

Key Points:

• Normal urine color: Pale to amber-yellow (due to urochrome).

• Abnormal colors:

  • Red: Hematuria, hemoglobinuria.

  • Brown-black: Melanin, alkaptonuria.

  • Green-blue: Pseudomonas infection, medications.

• Brown-black urine can be caused by melanin or its metabolites (e.g., melanogen), which oxidize upon exposure to air. This is seen in malignant melanoma with metastatic spread (melanuria).

• Other causes of dark urine include:

  • Hemoglobin/myoglobin: Reddish-brown (not true black).

  • Bilirubin: Dark amber/foamy (liver disease).

  • Alkaptonuria: Homogentisic acid turns black on standing (rare genetic disorder).

Why Not the Others?

• a) Hemoglobin: Causes red-brown urine (e.g., hemolysis).

• c) Myoglobin: Leads to reddish-brown urine (rhabdomyolysis).

• d) Bilirubin: Produces yellow-brown, foamy urine (hepatobiliary disease).

• Polyuria refers to a condition where there is a significant increase in urine output (typically more than 2.5–3 liters per day in adults). It can be caused by conditions like diabetes mellitus, diabetes insipidus, excessive fluid intake, or certain medications.

• Oliguria (a): This refers to decreased urine output (usually less than 400 mL per day in adults), often seen in dehydration, kidney failure, or urinary obstruction.

• Nocturia (b): This is the need to wake up at night to urinate frequently, but it doesn’t necessarily mean an overall increase in daily urine volume.

• Anuria (d): This is the absence or near-absence of urine output (less than 50–100 mL per day), indicating severe kidney dysfunction or obstruction.

• Dark yellow to amber-colored urine often suggests the presence of bilirubin, a yellow pigment derived from the breakdown of hemoglobin. When the liver cannot properly process bilirubin (as in hepatitis, cirrhosis, or bile duct obstruction), excess bilirubin is excreted in urine, giving it a darker, amber hue.

Why Not the Others?

• a) Urobilinogen – Normally present in small amounts and makes urine slightly yellow, but excessive amounts (e.g., in liver disease or hemolysis) may darken urine only after oxidation to urobilin (not typically amber).

• b) Protein – Proteinuria (e.g., due to kidney disease) does not directly affect urine color but may cause foamy urine.

• d) Hemoglobin – Causes red, pink, or cola-colored urine (hemoglobinuria), not amber.

• A refractometer determines specific gravity by measuring the refraction (bending) of light as it passes through urine.

  • Dissolved solutes in urine alter the speed of light, changing the refractive index.

  • The refractometer converts this optical change into a specific gravity value.

Why Not the Others?

• b) Color change: Used by reagent strips, not refractometers.

• c) Chemical reaction: Relevant for dipstick tests (e.g., ion-sensitive pads).

• d) Ion exchange: Part of electrode-based methods, not refractometry.

• Phenazopyridine (e.g., Pyridium, AZO) is a urinary analgesic frequently prescribed for cystitis (bladder inflammation/infection) to relieve pain and burning during urination. A hallmark side effect is bright orange or reddish-orange urine due to its dye properties .

• Mechanism: The drug is excreted unchanged in urine, staining it vividly. This is harmless but can be mistaken for blood .

Why Not the Others?

• a) Bilirubin: Causes dark amber/foamy urine (liver disease), not bright orange .

• c) Rifampin therapy: Turns urine reddish-orange but is used for tuberculosis, not cystitis.

• d) Ammonia: Causes pungent odor in UTIs but does not alter color .

Key Points:

• Clinical context: Phenazopyridine is specific to urinary symptoms (e.g., cystitis, UTIs), while rifampin is unrelated.

• Patient counseling: Warn patients about staining (clothing, contact lenses) and that it does not treat infection (requires antibiotics)

• Isosthenuria refers to urine with a fixed specific gravity (SG) of ~1.010, which matches the osmolality of plasma ultrafiltrate (~300 mOsm/kg). This occurs when the kidneys lose the ability to concentrate or dilute urine, typically due to:

  • Chronic kidney disease (CKD): Tubular damage impairs solute/water reabsorption.

  • Acute tubular necrosis (ATN): Temporary loss of tubular function.

Why Not the Others?

• a) 1.001: Seen in diabetes insipidus (hyposthenuria).

• c) 1.020: Indicates partial concentrating ability (e.g., mild dehydration).

• d) 1.040: Suggests artifact (e.g., radiocontrast dye) or extreme dehydration.

Key Points:

• Diagnostic significance:

  • Early CKD: Kidneys may still vary SG slightly.

  • Advanced CKD: SG becomes fixed at 1.010 (isosthenuria).

• Differentiation:

  • Hyposthenuria (SG <1.007): Diabetes insipidus.

  • Hypersthenuria (SG >1.030): Dehydration/glycosuria.

• Diurnal variation (daily fluctuations in urine composition) is best compensated by a 24-hour urine collection, which averages out these changes and provides a comprehensive assessment of solute excretion.

  • Clinical uses:

    • Proteinuria quantification (e.g., nephrotic syndrome).

    • Electrolyte/creatinine clearance (e.g., hypercalciuria, CKD staging).

  • Advantage: Eliminates timing biases (e.g., postprandial spikes in glucose/electrolytes).

Why Not the Others?

• a) Random sampling: Highly variable due to diet/activity (e.g., transient proteinuria after exercise).

• b) First-morning void: Assesses concentrating ability but misses daily fluctuations.

• d) Timed 2-hour sample: Too brief to account for diurnal patterns.

Key Points:

• Procedure:

  • Discard first morning void, then collect all urine for 24 hours.

  • Keep refrigerated to prevent degradation.

• Limitations:

  • Patient compliance (incomplete collections are common).

  • Alternatives: Spot urine protein-to-creatinine ratio (PCR) for estimating daily protein excretion.

• Anuria is defined as a severely reduced or absent urine output, specifically less than 100 mL per day. It indicates critical kidney failure or a complete blockage of urinary flow (e.g., from kidney stones, severe dehydration, or advanced renal disease).

Why Not the Others?

• a) Output >3 liters/day → This describes polyuria (excessive urine production).

• b) Nighttime urination → This is nocturia (frequent urination at night).

• d) Painful urination → This is dysuria (a symptom of UTI or other urinary tract issues).

Thus, anuria (c) is correctly defined as urine output <100 mL/day.

• Porphyrins are natural compounds produced during heme synthesis. In certain conditions like porphyria (a rare metabolic disorder), excessive porphyrins are excreted in urine, giving it a red or port-wine color. Importantly, standard urine dipstick tests for blood do not detect porphyrins, so the test will be negative despite the red discoloration.

Why Not the Others?

• a) Hemoglobin and b) Myoglobin

  • Both hemoglobin (from hemolysis) and myoglobin (from muscle breakdown) will cause a positive blood result on a urine dipstick because the test detects the heme group present in these proteins.

  • Hemoglobinuria makes urine red/pink, while myoglobinuria often turns it red-brown.

• d) Intact red blood cells (RBCs)

  • Microscopic hematuria (RBCs in urine) also triggers a positive dipstick test for blood.

n uncontrolled diabetes mellitus, excess glucose in the blood spills into the urine (glucosuria), pulling water with it due to osmotic diuresis. This leads to:

• Increased urine volume (polyuria), causing the urine to appear pale yellow

• Elevated specific gravity due to the presence of glucose, a solute that increases urine concentration despite dilution by water.

• Phenazopyridine, a urinary analgesic (e.g., Pyridium), is a well-known cause of bright orange or orange-red urine. This is a harmless and expected side effect of the medication.

• Other causes of orange urine include dehydration (concentrated urochrome) or excess bilirubin (liver disease).

Why Not the Others?

• a) Hematuria – Typically causes red, pink, or cola-colored urine, not orange.

• b) Urobilinogen – In normal amounts, it contributes to yellow urine; excess urobilinogen may darken urine but not specifically turn it orange.

• d) Proteinuria – Does not change urine color; may cause foamy urine but not discoloration.

• The yellow color of urine is primarily due to urochrome, a pigment produced from the breakdown of hemoglobin during the normal destruction of aged red blood cells. Urochrome is excreted by the kidneys and gives urine its characteristic yellow hue.

Why Not the Others?

• a) Hemoglobin – If present in urine (hemoglobinuria), it would make urine appear red or cola-colored, not the normal yellow.

• b) Bilirubin – Excess bilirubin (e.g., in liver disease) can make urine dark amber or brownish, but it is not responsible for the typical yellow color.

• d) Porphyrins – These are rare metabolic byproducts; if excreted in excess (porphyria), urine may appear red or purple, not normal yellow.

• Osmolality measures the total number of solute particles per kilogram of water, including:

  • Ions (e.g., Na⁺, K⁺, Cl⁻).

  • Molecules (e.g., glucose, urea).

  • Proteins and other dissolved substances.

• It is the gold standard for assessing urine/plasma concentration, unaffected by solute size or type.

Why Not the Others?

• b) Non-ionized molecules: Osmolality includes both ionized and non-ionized solutes.

• c) Sodium chloride content: Only a subset; osmolality accounts for all solutes, not just NaCl.

• d) Ionic compounds only: Incorrect; osmolality also measures non-ionic solutes (e.g., glucose).

Key Points:

• Clinical uses:

  • Urine osmolality: Evaluates renal concentrating ability (e.g., diabetes insipidus).

  • Serum osmolality: Detects imbalances (e.g., hypernatremia, toxic alcohol ingestion).

• Osmolal gap: Difference between measured and calculated osmolality (elevated in methanol/ethylene glycol poisoning).

• Diabetes insipidus (DI) causes dilute, pale yellow or colorless urine due to the kidneys’ inability to concentrate urine. This results from:

  • Central DI: Deficiency of antidiuretic hormone (ADH).

  • Nephrogenic DI: Renal resistance to ADH.

• The urine has low specific gravity (SG <1.005) and high volume (polyuria) because excessive water is excreted.

Why Not the Others?

• b) Yellow: Normal urine color, seen with adequate hydration.

• c) Dark yellow: Indicates concentrated urine (e.g., dehydration), the opposite of DI.

• d) Brown: Suggests bilirubinuria (liver disease) or myoglobinuria (rhabdomyolysis).

Key Points:

• Clinical triad: Polyuria, polydipsia, pale urine.

• Diagnostic tests:

  • Water deprivation test: Confirms inability to concentrate urine.

  • Response to desmopressin: Distinguishes central vs. nephrogenic DI.

• Specific gravity (SG) directly measures the density of urine compared to water, reflecting its concentration of solutes (e.g., electrolytes, urea). It is the primary clinical term for assessing urine concentration.

  • Low SG (~1.001–1.010): Dilute urine (e.g., overhydration, diabetes insipidus).

  • High SG (>1.030): Concentrated urine (e.g., dehydration, SIADH).

Why Not the Others?

• a) Osmolality: While more precise (measures solute particles/kg water), it requires specialized labs and is not routine in urinalysis.

• c) pH: Indicates acidity/alkalinity, not concentration.

• d) Turbidity: Describes cloudiness, unrelated to solute concentration.

Key Points:

• SG correlates with osmolality but is affected by large molecules (e.g., glucose, protein).

• Refractometers or reagent strips are used for SG measurement.

• A refractometer measures urine specific gravity by assessing light refraction as it passes through the sample. The refractive index changes with solute concentration, providing an SG value.

  • Advantages: Requires only 1–2 drops of urine, unaffected by temperature.

  • Limitations: Less accurate for high glucose/protein (unlike osmometry).

Why Not the Others?

• a) Osmometer: Measures osmolality (solute particles/kg water), not SG.

• b) Urinometer: Uses buoyancy (floats in urine), but requires large volume and temperature correction.

• d) Densitometer: A general term for density measurement; not specific to clinical urinalysis.

Key Points:

• Refractometers are standard in labs due to speed and convenience.

• Reagent strips estimate SG but rely on ionic concentration, missing non-ionic solutes.

• Low urine specific gravity (SG <1.005) suggests dilute urine, most commonly caused by:

  • Diabetes insipidus (DI): Either central (ADH deficiency) or nephrogenic (kidney resistance to ADH), leading to inability to concentrate urine.

  • Excessive water intake (psychogenic polydipsia): The kidneys excrete large volumes of dilute urine to compensate.

Why Not the Others?

• a) Diabetes mellitus: Causes high SG due to glycosuria (glucose increases urine density).

• b) Heart failure: Typically leads to high SG from fluid retention and concentrated urine.

• d) Dehydration: Results in high SG (>1.030) as kidneys conserve water.

• Urochrome is the primary pigment responsible for the yellow color of urine. It is a byproduct of hemoglobin breakdown and is excreted by the kidneys at a relatively constant rate.

• The shade of yellow varies with hydration status:

  • Dilute urine (pale yellow): High water content.

  • Concentrated urine (dark yellow/amber): Low water content (e.g., dehydration).

Why Not the Others?

• a) Hemoglobin: Causes red/brown urine if present (hematuria or hemoglobinuria).

• b) Urobilin: A derivative of bilirubin that contributes to yellow-brown color in feces, not urine.

• d) Bilirubin: Imparts a dark amber/foamy appearance in liver disease but is not the normal yellow pigment.

Key Points:

• Urochrome levels are stable, making urine color a quick hydration indicator.

• Abnormal colors (e.g., blue, green) are typically due to medications, infections, or metabolic disorders.

• pH is a chemical property of urine, not a physical one. It measures the acidity or alkalinity of urine and requires a chemical test (dipstick or pH meter) for assessment.

Physical Properties of Urine (Observed Directly):

• b) Color: Visible appearance (e.g., yellow, red, brown).

• c) Clarity: Transparency (clear, hazy, cloudy).

• d) Specific gravity: Density relative to water (measured via refractometer or dipstick).

Key Points:

• Chemical properties (e.g., pH, glucose, protein) require reagent strips or lab tests.

• Physical vs. chemical:

  • Physical: Observed/measured without altering composition.

  • Chemical: Involves reactions (e.g., pH indicators).

• A strong ammonia odor in urine is most commonly caused by bacterial breakdown of urea into ammonia, which occurs when urine is left standing at room temperature for an extended period. This is a normal process and does not indicate disease.

• In freshly voided urine, a strong ammonia smell may also suggest dehydration (highly concentrated urine) or a diet high in protein.

Why Not the Others?

• a) Contamination: While bacteria can cause odor, “contamination” alone is too vague (e.g., vaginal bacteria may cause other smells).

• c) Hepatic disease: Typically causes a musty/mousy odor (due to elevated bilirubin metabolites), not ammonia.

• d) Diabetes mellitus: Produces a fruity odor (ketones), not ammonia.

Key Points:

• UTI consideration: If fresh urine smells strongly of ammonia, test for infection (e.g., Proteus bacteria, which hydrolyze urea rapidly).

• Benign vs. pathologic:

  • Benign: Ammonia smell in old or concentrated urine.

  • Concerning: Persistent ammonia odor + dysuria/cloudiness (UTI).

• Refractometer measurements of specific gravity (SG) must be corrected for high glucose levels because glucose disproportionately increases the refractive index, leading to falsely elevated SG values.

  • Correction formula: Adjusted SG = Measured SG – (0.004 × [glucose in g/dL]).

  • Example: If SG = 1.030 and glucose = 2 g/dL, corrected SG = 1.030 – 0.008 = 1.022.

Why Not the Others?

• a) Ambient temperature: Refractometers are temperature-compensated (unlike urinometers).

• b) Atmospheric pressure: Negligible effect on refractive index in clinical settings.

• d) Specimen volume: Refractometers need only 1–2 drops (volume irrelevant).

Key Points:

• Proteinuria also requires correction (1 g/dL protein ≈ +0.003 SG).

• Clinical impact: Uncorrected high glucose/protein can mask isosthenuria (fixed SG 1.010 in renal disease).

• Urine pH directly influences crystal formation:

  • Acidic urine (pH <6): Promotes uric acid and calcium oxalate crystals.

  • Alkaline urine (pH >7): Favors triple phosphate (struvite) and calcium phosphate crystals.

• This is critical for managing kidney stone risk (e.g., alkalinizing urine to prevent uric acid stones).

Why Not the Others?

• a) Color: Primarily determined by urochrome, bilirubin, or blood (pH has minimal effect).

• b) Odor: Depends on bacterial metabolism (e.g., ammonia in UTIs) or diet, not pH.

• d) Specific gravity: Measures solute concentration, unrelated to pH.

Key Points:

• Clinical relevance:

  • UTI with Proteus: Alkaline urine + struvite crystals.

  • Gout: Acidic urine + uric acid crystals.

• Therapeutic urine pH adjustment is used for stone prevention.

• The first-morning urine sample is optimal for assessing renal concentrating ability because:

  • It is naturally concentrated after overnight fasting (8+ hours without fluid intake), maximizing solute retention.

  • Reflects the kidney’s peak concentrating capacity (specific gravity typically >1.020 in healthy adults).

• Clinical use: Evaluates for:

  • Diabetes insipidus (SG <1.005 despite dehydration).

  • Chronic kidney disease (isosthenuria: fixed SG ~1.010).

Why Not the Others?

• a) Random urine: Affected by recent fluid intake/food (variable SG).

• c) Post-meal sample: May be diluted by prandial fluid intake.

• d) 24-hour collection: Measures total solute excretion (e.g., protein, creatinine) but not concentrating ability.

Key Points:

• Procedure:

  • Collect immediately upon waking (no prior fluid intake).

  • Test specific gravity or osmolality (gold standard).

• Limitations:

  • Elderly patients: Reduced concentrating ability (SG may be lower).

  • Contaminants: Vaginal secretions/mucus can affect clarity.

• Suprapubic aspiration is the most sterile method of urine collection because it involves inserting a needle directly into the bladder through the abdominal wall, bypassing the urethra and vaginal flora, which are common sources of contamination in other methods.

• This technique is particularly useful for infants, patients with UTIs unresponsive to treatment, and when culturing anaerobic bacteria.

Why Not the Others?

• a) Random void: Highly prone to contamination from genital flora.

• b) Catheterization: Sterile but carries a risk of introducing bacteria into the bladder (catheter-associated UTI).

• d) Midstream clean-catch: Reduces contamination but not as sterile as suprapubic aspiration.

Key Points:

• Clinical use:

  • Gold standard for diagnosing UTIs in neonates.

  • Reserved for cases where absolute sterility is critical.

• Limitations: Invasive, requires clinical expertise.

• Reagent strips for specific gravity (SG) primarily measure ionic solutes (e.g., Na⁺, K⁺, Cl⁻) via a polyelectrolyte system that releases hydrogen ions in proportion to urine ion concentration.

  • The pH-sensitive dye (e.g., bromothymol blue) changes color based on H⁺ release, correlating with SG.

Why Not the Others?

• a) Glucose concentration: Detected by a separate glucose pad on the strip, not the SG pad.

• c) All solutes: Refractometers detect all solutes; reagent strips miss non-ionic solutes (e.g., glucose, urea).

• d) Proteins: Measured by the protein pad (albumin-specific); they minimally affect SG strips.

Key Points:

• Limitation: Reagent strips underestimate true SG if urine contains non-ionic solutes (e.g., high glucose in diabetes).

• Refractometers are more accurate for clinical decisions.

• Midstream clean-catch urine is the preferred method for ambulatory patients with suspected UTIs because it balances sterility and practicality. Key advantages include:

  • Minimized contamination: The first few milliliters of urine flush out urethral contaminants, and the midstream portion is collected in a sterile container .

  • Non-invasive: Avoids risks associated with catheterization (e.g., trauma, infection) or suprapubic aspiration (reserved for infants or complex cases).

  • Guideline-backed: Recommended by protocols for adults and toilet-trained children when UTI is suspected .

Why Not the Others?

• a) Random void: High risk of contamination from genital flora, reducing diagnostic accuracy .

• b) Catheterization: Used for non-ambulatory or catheterized patients but carries risks (e.g., CAUTI) and is unnecessary for most ambulatory cases .

• c) Suprapubic aspiration: Reserved for infants, critically ill patients, or when other methods fail .

Key Points:

• Preparation: Patients should clean the perineal/urethral area before collection to reduce contamination .

• Exceptions:

  • Men with low-risk UTIs: Midstream clean-catch suffices .

  • Recurrent/complicated UTIs: May require catheterization or imaging

• Dark amber urine with yellow foam is a classic sign of bilirubinuria, caused by excess conjugated bilirubin (liver disease or biliary obstruction). The foam appears yellow due to bilirubin’s pigment.

• Mechanism: Bilirubin reduces urine surface tension, creating persistent foam (unlike the transient bubbles of normal urine).

Why Not the Others?

• a) Urobilinogen: Causes normal yellow urine; no foam.

• c) Hemoglobin: Produces red-brown urine (positive dipstick but no foam).

• d) Myoglobin: Leads to reddish-brown urine (rhabdomyolysis), but foam is atypical.

Key Points:

• Confirmatory tests:

  • Dipstick: Positive for bilirubin (reacts with diazo dye).

  • Ictotest: More specific for bilirubin.

• Clinical correlation: Jaundice, pale stools, and pruritus support hepatobiliary disease.

• Refrigeration (2–8°C) is the standard method to preserve urine samples for delayed analysis (>1 hour). It slows:

  • Bacterial growth (prevents false-positive nitrites/cloudiness).

  • Degradation of cells (RBCs/WBCs) and casts.

  • Chemical changes (e.g., pH rise from urea breakdown).

• Shelf life: Up to 24 hours if refrigerated (though ideally tested within 4–6 hours) .

Why Not the Others?

• a) Frozen: Destroys cells and casts (ice crystals cause lysis).

• c) Acidified: Used only for specific tests (e.g., urobilinogen) but alters pH and harms cells.

• d) Discarded: Unnecessary; refrigeration maintains sample integrity .

Key Points:

• Pre-refrigeration steps:

  • Label and seal the container.

  • Record time of collection/refrigeration.

• Post-refrigeration: Warm to room temperature before testing to dissolve crystals (e.g., urates) .

• A discrepancy between refractometer-specific gravity (high) and dipstick-specific gravity (normal) often occurs with proteinuria because:

  • Refractometers detect all solutes, including proteins, which increase refractive index.

  • Dipsticks measure ionic concentration (Na⁺, K⁺, Cl⁻) and miss non-ionic proteins, underestimating true SG.

• Nephrotic syndrome is a classic example (heavy proteinuria with normal dipstick SG).

Why Not the Others?

• b) Hypernatremia: Elevates both refractometer and dipstick SG (high ionic solutes).

• c) Acidosis: No direct effect on SG measurements.

• d) Ketonuria: Dipsticks detect ketones, but they contribute minimally to SG.

Key Points:

• Confirmatory tests:

  • Urine protein-to-creatinine ratio (UPCR) or 24-hour urine protein.

  • Sulfosalicylic acid test for non-albumin proteins.

• Clinical relevance:

  • Glomerular diseases (e.g., diabetic nephropathy) often cause this pattern.

• Porphyrins (e.g., in porphyria) can cause red urine but do not react with the heme-peroxidase reagent on urine dipsticks (which detects hemoglobin/myoglobin).

• Other dipstick-negative red urine causes:

  • Dietary pigments (beets, blackberries).

  • Drugs (rifampin, phenazopyridine).

Why Not the Others?

• a) Hematuria: Dipstick positive for blood (RBCs contain hemoglobin).

• b) Myoglobin and d) Hemoglobin: Both trigger a positive blood result (dipstick detects heme groups).

Key Points:

• Porphyria diagnosis:

  • Urine porphobilinogen (PBG) test (Watson-Schwartz test).

  • UV light shows pink fluorescence in porphyrin-rich urine.

• Clinical clues:

  • Porphyria: Abdominal pain, neuropsychiatric symptoms.

  • Beeturia: Harmless, affects ~10–14% of people.

• Maple syrup urine disease (MSUD) is named for its hallmark sweet, maple syrup-like odor in urine, sweat, and earwax. This distinctive smell is caused by the accumulation of branched-chain amino acids (leucine, isoleucine, valine) and their byproducts, particularly sotolone (4,5-dimethyl-3-hydroxy-2[5H]-furanone), a compound also found in fenugreek and maple syrup .

Why Not the Others?

• a) Fruity: Associated with ketones (e.g., diabetic ketoacidosis).

• b) Musty: Linked to phenylketonuria (PKU) or liver disease.

• c) Ammoniacal: Typical of UTIs (bacterial urea breakdown).

Key Points:

• The odor is often detectable within 12–24 hours after birth in classic MSUD .

• Diagnostic clue: The scent is most noticeable in dried urine (e.g., on a diaper)

• The refractive index measures how much light slows down when passing from air into a solution (e.g., urine). It is calculated as:

  Refractive index=Speed of light in airSpeed of light in the solutionRefractive index=Speed of light in the solutionSpeed of light in air​

• In urinalysis, refractometers use this principle to estimate specific gravity (density of solutes in urine).

Why Not the Others?

• a) Speed in solutions vs. solids: Irrelevant to clinical refractometry.

• c) Scatter in air vs. solutions: Describes turbidimetry, not refraction.

• d) Scatter by solutes: Refers to light scattering techniques (e.g., nephelometry), not refractive index.

Key Points:

• Higher solute concentration = greater refractive index = higher specific gravity.

• Clinical utility:

  • Detects all solutes (unlike reagent strips, which miss non-ionic molecules).

  • Requires only 1–2 drops of urine.

• The normal yellow color of urine is primarily due to urochrome, a pigment derived from the breakdown of hemoglobin during the normal turnover of red blood cells. Urochrome is excreted by the kidneys at a relatively constant rate, giving urine its characteristic hue.

• The shade of yellow varies with hydration:

  • Pale yellow: Dilute urine (high water intake).

  • Dark yellow/amber: Concentrated urine (dehydration).

Why Not the Others?

• b) Melanin: Causes black urine in rare cases of malignant melanoma (melanuria).

• c) Bilirubin: Leads to dark amber/foamy urine in liver disease (bilirubinuria).

• d) Stercobilin: The pigment responsible for brown stool color, not urine.

Key Points:

• Urochrome production is constant, making urine color a quick indicator of hydration status.

• Abnormal colors (e.g., red, blue, green) typically result from medications, diet, or pathology (e.g., blood, infections).

• Reagent strips for specific gravity (SG) primarily detect ionic solutes (e.g., Na⁺, K⁺, Cl⁻) and do not respond to non-ionic solutes like glucose or urea.

  • In conditions with high glucose (e.g., diabetes mellitus), the true SG is higher than what the strip indicates because glucose contributes to urine density but is not detected by the ionic pad.

Why Not the Others?

• a) High protein concentration: May slightly increase SG (1 g/dL protein ≈ +0.003 SG), but strips are less affected than refractometers.

• b) Low pH: Does not interfere with SG measurement (strips compensate for pH variations).

• d) High temperature: Affects urinometers but not reagent strips (which are temperature-stable).

Key Points:

• Refractometers are preferred for urine with high glucose/protein as they measure all solutes.

• Clinical correlation: In diabetes, always correlate SG with glucose dipstick results.

• Specific gravity (SG) is a key test for renal tubular function, as it reflects the kidneys’ ability to concentrate or dilute urine by reabsorbing water and solutes.

  • Normal response: Varies SG based on hydration (1.005–1.030).

  • Tubular dysfunction:

    • Isosthenuria (fixed SG ~1.010) suggests chronic kidney disease or tubular damage.

    • Hyposthenuria (SG <1.007) indicates diabetes insipidus (tubular resistance to ADH).

Why Not the Others?

• a) Creatinine clearance: Measures glomerular filtration rate (GFR), not tubular function.

• c) Urea nitrogen: Reflects protein metabolism and GFR, not tubular health.

• d) Daily volume: Non-specific; polyuria/oliguria have many causes.

Key Points:

• Confirmatory tests:

  • Water deprivation test: Evaluates maximal urine concentration.

  • Urine osmolality: More precise than SG for tubular assessment.

• Clinical correlation:

  • Acute tubular necrosis (ATN): Isosthenuria + muddy brown casts.

  • Fanconi syndrome: Low SG + glycosuria/aminoaciduria.

• Microscopic examination is the gold standard for identifying the cause of urine turbidity. It can distinguish:

  • WBCs (infection).

  • RBCs (hematuria).

  • Crystals (urate, phosphate).

  • Bacteria or yeast.

  • Mucus or contaminants.

Why Not the Others?

• a) Discard the sample: Unnecessary without investigation.

• b) Chemical test for protein: Detects proteinuria but not the cause of cloudiness (e.g., crystals vs. cells).

• d) Refrigerate the specimen: Preserves the sample but does not diagnose turbidity.

Key Points:

• Centrifugation enhances microscopic analysis by concentrating sediment.

• Dipstick first: If positive for leukocyte esterase/nitrites, suggests infection (but microscopy confirms).

Transient postprandial cloudiness in urine with a normal dipstick is typically due to amorphous phosphates, which can precipitate in alkaline urine after eating (the alkaline tide effect). This is a benign finding and often resolves without intervention.

Why Not the Others?

• a) Bacteriuria: Would typically cause persistent cloudiness + positive leukocyte esterase/nitrites on dipstick 19.

• b) Pyuria: Indicates WBCs (infection/inflammation), causing cloudiness with positive leukocyte esterase 48.

• d)  Transient postprandial cloudiness (cloudy urine after eating) with a normal dipstick (no leukocyte esterase, nitrites, or blood) is most commonly caused by amorphous urates.

• Normal urine odor is caused by the breakdown of urea into ammonia by bacteria, which occurs gradually after urine is voided. Fresh urine typically has a mild, inoffensive smell, but it develops a stronger ammonia-like odor over time due to this process.

Why Not the Others?

• a) Ketones: Produce a fruity/sweet smell (e.g., diabetic ketoacidosis) — not normal.

• b) Bacteria: Only contribute to odor if a UTI is present (foul-smelling urine).

• c) Ammonia: While ammonia is a product of urea breakdown, it is not the primary source of fresh urine odor.

Key Points:

• Diet and medications can alter urine odor (e.g., asparagus, antibiotics).

• Strong ammonia odor in fresh urine may suggest dehydration (highly concentrated urine) or infection (if accompanied by other symptoms).

• Refractometers are ideal for measuring specific gravity (SG) in very small urine volumes (as little as 1–2 drops) because they analyze light refraction through the sample.

• They are fast, temperature-stable, and widely used in clinical labs.

Why Not the Others?

• a) Urinometer: Requires 10–15 mL of urine (impractical for small volumes).

• b) Dipstick: Needs ~1 mL but is less accurate (measures only ionic solutes, missing glucose/protein).

• d) Gravimetric method: Precise but labor-intensive and requires larger volumes (not routine in clinics).

Key Points:

• Refractometer advantages:

  • Detects all solutes (unlike dipsticks).

  • No calibration needed for small samples.

• Neonatal/pediatric use: Preferred due to low sample requirements

Polyuria (excessive urine output, typically >3L/day) can be caused by:

1. Diabetes mellitus – High blood glucose leads to osmotic diuresis (excess glucose spills into urine, pulling water with it).

2. Diabetes insipidus – Either a lack of ADH (central DI) or kidney resistance to ADH (nephrogenic DI), resulting in large volumes of dilute urine.

3. Excessive fluid intake (psychogenic polydipsia) – The body excretes more urine to manage the excess water.

4. Diuretic medications – Increase urine production.

Why Not the Others?

• a) Dehydration → Typically causes oliguria (low urine output) as the body conserves water.

• b) Congestive heart failure → Often leads to fluid retention and reduced urine output due to poor kidney perfusion.

• d) Shock → Usually results in decreased urine output (oliguria or anuria) due to low blood flow to the kidneys.

• Distilled water (or deionized water) is the standard solution for calibrating a refractometer because it has a known specific gravity of 1.000 at a specified temperature (usually 20°C or 25°C).

  • The refractometer is adjusted to read 1.000 when water is applied, ensuring accuracy for subsequent urine measurements.

Why Not the Others?

• a) Urine control: Used for quality control (verifying performance) but not calibration.

• b) Sodium chloride: Has a higher SG (~1.022 for 5% NaCl), making it unsuitable for zero-point calibration.

• d) Sucrose solution: Used for industrial refractometers (e.g., food industry), not medical urine analysis.

Key Points:

• Calibration steps:

  1. Place distilled water on the refractometer prism.

  2. Adjust the scale to read 1.000.

  3. Wipe dry and test urine samples.

• Specific gravity (SG) directly assesses the kidney’s ability to concentrate urine by measuring the density of solutes (e.g., electrolytes, urea) relative to water.

  • Normal range: 1.005–1.030.

  • High SG (>1.030): Indicates concentrated urine (e.g., dehydration, SIADH).

  • Low SG (<1.005): Suggests dilute urine (e.g., diabetes insipidus, overhydration).

Why Not the Others?

• a) Filtration capacity: Assessed by GFR (e.g., creatinine clearance).

• c) Erythropoietin synthesis: Unrelated to SG; evaluated via serum EPO levels.

• d) Waste excretion: Indirectly reflected but not quantified by SG alone.

Key Points:

• Isosthenuria (fixed SG ~1.010): Indicates renal tubular dysfunction (e.g., chronic kidney disease).

• Limitations: SG is affected by non-renal factors (e.g., glycosuria, radiocontrast dyes).

• The normal reference range for urine specific gravity (SG) in adults is 1.005–1.030, though this can vary slightly between laboratories.

  • 1.005–1.010: Indicates dilute urine (e.g., high fluid intake, diabetes insipidus).

  • 1.010–1.020: Typical for random samples in well-hydrated individuals.

  • 1.025–1.030: Suggests concentrated urine (e.g., dehydration, SIADH).

Why Not the Others?

• b) 1.000–1.020: Too narrow; excludes normal concentrated urine.

• c) 1.010–1.040: Includes abnormally high values (>1.035 is rare and may indicate artifacts like radiocontrast dye).

• d) 1.015–1.025: Too restrictive; misses normal hydration extremes.

• Milky white urine is most characteristic of chyluria, caused by lymphatic fluid (chyle) leaking into the urinary tract. This occurs due to:

  • Lymphatic obstruction (e.g., filariasis, trauma, or tumors).

  • Chyle contains fat droplets (triglycerides), giving urine a milky appearance.

Why Not the Others?

• a) Hematuria: Causes red/brown urine, not milky.

• b) Pyuria (WBCs in urine): Leads to cloudy urine, but not truly milky (unless pus is abundant, as in pyonephrosis).

• d) Phosphaturia: Causes white precipitate in alkaline urine, but dissolves with acetic acid (unlike chyluria).

Key Points:

• Confirmation of chyluria:

  • Ether extraction test: Urine clears when mixed with ether (fat-soluble).

  • Sudan III stain: Detects fat globules.

• Filariasis: The most common global cause (endemic regions).

• Rifampin, an antibiotic used for tuberculosis, is a classic cause of bright orange urine due to its natural pigment. This is a harmless side effect.

• Other medications (e.g., phenazopyridine) and foods (e.g., carrots) can also cause orange urine.

Why Not the Others?

• a) Hematuria: Causes red/pink urine (unless old blood turns brown).

• c) Diabetes insipidus: Leads to colorless, dilute urine (low specific gravity).

• d) High bilirubin: Produces dark amber/foamy urine, not orange.

Key Points:

• Orange urine differential:

  • Medications: Rifampin, sulfasalazine.

  • Dehydration: Concentrated urochrome (dark yellow-orange).

  • Liver disease: Bilirubin + urobilinogen (amber/orange-brown).

• Reddish-brown urine after trauma (e.g., crush injury, burns, or strenuous exercise) strongly suggests rhabdomyolysis, where muscle damage releases myoglobin into the bloodstream. Myoglobin is filtered by the kidneys, turning urine reddish-brown (“cola-colored”).

  • Dipstick: Positive for blood (heme reaction) but no RBCs on microscopy.

  • Serum tests: Elevated creatine kinase (CK) (>5,000 U/L).

Why Not the Others?

• a) Stercobilin: A fecal pigment (brown stool), irrelevant to urine.

• b) Porphyrinogens: Cause port-wine/black urine in porphyria, unrelated to trauma.

• d) Fresh erythrocytes: Produce bright red/pink urine (hematuria), not brown.

Key Points:

• Clinical urgency: Myoglobin can cause acute kidney injury (tubular necrosis).

• Differential:

  • Hemoglobinuria (intravascular hemolysis): Similar color but with low haptoglobin.

  • Hematuria: RBCs on microscopy.

• Reagent strip SG testing relies on a pH-sensitive dye (e.g., bromothymol blue) and a polyelectrolyte.

  • Principle: The polyelectrolyte releases H⁺ ions in response to urine cations (Na⁺, K⁺).

  • The pH change alters the dye’s color (e.g., blue-green to yellow), correlating with ionic concentration (SG).

Why Not the Others?

• a) Conductivity: Used by electrolyte analyzers, not SG strips.

• c) Turbidity measurement: Irrelevant to reagent strips.

• d) Refractive index: The basis for refractometers, not strips.

Key Points:

• Limitation: Strips detect only ions, missing non-ionic solutes (e.g., glucose, urea).

• Clinical tip: Use refractometers for accurate SG in glycosuria/proteinuria.

• Urine clarity (described as clear, hazy, cloudy, or turbid) should be assessed immediately after collection while the sample is fresh and at room temperature.

• This timing is critical because:

  • Refrigeration (d) can cause dissolved solutes (e.g., phosphates, urates) to precipitate, artificially increasing cloudiness.

  • Centrifugation (a) alters the sample by sedimenting particles, making the supernatant appear clearer than the original urine.

  • Chemical testing (b) may change urine composition (e.g., pH shifts affecting crystal formation).

Why Immediate Assessment Matters:

• Fresh urine reflects the true clinical state (e.g., infection-related WBCs/bacteria cause persistent cloudiness, while crystals may form later).

• Delayed evaluation can lead to false interpretations (e.g., mistaking refrigeration-induced crystals for pyuria).

Post-exposure black urine discoloration is characteristic of alkaptonuria, a rare metabolic disorder caused by a deficiency of the enzyme homogentisate oxidase. This leads to the accumulation of homogentisic acid, which oxidizes upon standing or exposure to air, turning the urine black.

Why Not the Others?

• a) Bile pigments: Cause dark amber/foamy urine (e.g., bilirubin in liver disease) but do not darken post-exposure 47.

• c) Post-exposure black urine discoloration (urine turning black after standing in air/light) is a classic sign of porphyria, where porphyrin precursors (e.g., porphobilinogen) oxidize into dark pigments like uroporphyrin or melanin-like compounds

• d) Hematuria: Produces red/brown urine (from RBCs/hemoglobin) that does not darken further with air exposure

• Oliguria refers to a decreased urine output, typically defined as less than 400 mL per day in adults (or <0.5 mL/kg/hour). It can result from dehydration, kidney dysfunction, heart failure, or urinary obstruction.

Why not the others?

• Anuria (b): This is a complete or near-complete absence of urine output (<50–100 mL per day), indicating severe kidney failure or obstruction.

• Enuresis (c): This refers to involuntary urination, especially at night (bedwetting), unrelated to urine volume.

• Nocturia (d): This is frequent urination at night but does not imply reduced total daily output.

Thus, Oliguria (a) is the correct term for decreased urine output.

• Alkaptonuria is a rare inherited disorder where urine turns dark brown or black upon standing due to the oxidation of homogentisic acid (HGA) in the urine when exposed to air. This occurs because of a deficiency of the enzyme homogentisate 1,2-dioxygenase, leading to HGA accumulation .

• Key features:

  • Urine darkening: Noticeable after several hours of standing (e.g., on a diaper or in a container).

  • Ochronosis: Later in life, HGA deposits in connective tissues (e.g., joints, ears) cause blue-black pigmentation and arthritis .

Why Not the Others?

• a) Phenylketonuria (PKU): Causes musty-smelling urine (due to phenylalanine metabolites) but no color change upon standing .

• c) Maple syrup urine disease: Urine smells sweet (like maple syrup) but does not darken .

• d) Diabetic ketoacidosis (DKA): Produces fruity-smelling urine (ketones) but no darkening .

Key Points:

• Diagnosis:

  • Urine HGA quantification (elevated).

  • Ferric chloride test: Urine turns black upon addition .

• Treatment: No cure, but low-protein diet (especially phenylalanine/tyrosine) may slow progression .

• Hyposthenuria (urine specific gravity <1.007) is classic for diabetes insipidus (DI), where the kidneys cannot concentrate urine due to:

  • Central DI: Lack of ADH (vasopressin) production (e.g., pituitary damage).

  • Nephrogenic DI: Renal resistance to ADH (e.g., lithium toxicity, genetic defects).

• Patients excrete large volumes of dilute urine (polyuria), regardless of hydration status.

Why Not the Others?

• a) Diabetes mellitus: Causes high SG from glycosuria (glucose increases urine density).

• c) Acute glomerulonephritis: Typically presents with hematuria/proteinuria, not dilute urine.

• d) Hepatic failure: May cause bilirubinuria but does not lower SG.

Key Points:

• Water deprivation test distinguishes central vs. nephrogenic DI.

• Psychogenic polydipsia also causes dilute urine but resolves with water restriction.

• Normal urine can appear hazy or slightly cloudy due to mucus secreted by the urinary tract (especially in women, due to vaginal or urethral secretions). This is physiologic and not indicative of disease.

Why Not the Others?

• a) Crystals: May cause cloudiness, but their presence (e.g., phosphates, urates) often suggests abnormal solute concentration or pH, not “normal” urine.

• c) Bacteria: Indicates infection (e.g., UTI), not normal urine.

• d) WBCs (Pyuria): Always pathologic (e.g., UTI, inflammation).

• A strong ammonia-like odor in urine is classic for bacterial UTIs (e.g., Proteus, E. coli). These bacteria hydrolyze urea into ammonia, creating the pungent smell.

• Other causes:

  • Dehydration: Concentrated urine can smell ammonia-like but lacks other UTI symptoms (e.g., dysuria).

  • Dietary factors: Asparagus, high-protein meals.

Why Not the Others?

• b) Diabetes mellitus: Causes fruity-smelling urine (ketones in DKA).

• c) Liver disease: Leads to musty/mousy odor (bilirubin metabolites).

• d) Starvation: Produces ketones (sweet/fruity odor), not ammonia.

The typical daily urine output for a healthy adult is 800–2,000 mL per day, with an average of about 1,500 mL. This range ensures proper excretion of waste products while maintaining hydration.

• Less than 400 mL/day (oliguria) may indicate dehydration or kidney dysfunction.

• More than 2,500 mL/day (polyuria) may suggest excessive fluid intake, diabetes, or other medical conditions.

• Clarity in urinalysis refers to the transparency of urine, described as:

  • Clear: No visible particulates.

  • Hazy: Slight cloudiness (e.g., mucus).

  • Cloudy/Turbid: Obscured visibility (e.g., WBCs, bacteria, crystals).

Why Not the Others?

• a) Color: Evaluated separately (e.g., yellow, red, brown).

• b) Foam presence: Assessed for proteinuria (not clarity).

• d) Odor: Noted for infections/metabolic disorders (e.g., ammonia in UTIs, fruity ketones).

Key Points:

• Common causes of turbidity:

  • Infection: WBCs, bacteria.

  • Crystals: Phosphates (alkaline urine), urates (acidic urine).

  • Contaminants: Mucus, semen.

• Clinical relevance: Cloudy urine + dysuria suggests UTI.

• Reagent strip tests for specific gravity (e.g., multistix) measure ionic concentration (mainly Na⁺, K⁺, Cl⁻) via a polyelectrolyte-based pH indicator system.

  • The strip contains a pH-sensitive dye (e.g., bromothymol blue) and a polyelectrolyte that releases H⁺ ions in response to urine cations.

  • More ions → more H⁺ release → pH change → color shift (green to blue).

Why Not the Others?

• a) Osmotic pressure: While related, strips do not directly measure it.

• c) Refractive index: Used by refractometers (a lab method), not strips.

• d) Density: Measured by urinometers (not strips).

• Specific gravity (SG) measures the density of urine compared to water, reflecting the total concentration of dissolved solutes (e.g., electrolytes, urea, glucose). It indirectly indicates the osmolality (number of solute particles per kilogram of water), which is a key marker of the kidney’s concentrating ability.

Why Not the Others?

• a) Color intensity – While concentrated urine (high SG) may appear darker, color is influenced by pigments (e.g., urochrome) unrelated to solute concentration.

• c) Clarity – Cloudiness depends on suspended particles (e.g., cells, crystals), not dissolved solutes.

• d) Protein concentration – Proteinuria can slightly increase SG, but SG primarily reflects small solutes (e.g., Na⁺, urea). Protein is better measured by dipstick or chemical tests.

• Distilled water has a specific gravity (SG) of 1.000 at standard room temperature (20–25°C) because it contains no dissolved solutes.

  • This value serves as the baseline for calibration of refractometers and urinometers.

Why Not the Others?

• a) 0.000: Impossible; SG is a ratio relative to water (which cannot be “0”).

• c) 1.005 or d) 1.010: Indicate solute presence (e.g., electrolytes), which distilled water lacks.

Key Points:

• Calibration: Refractometers must read 1.000 with distilled water to ensure accuracy.

• Temperature note: If water is not at the instrument’s specified temperature, minor adjustments may be needed.

• Refractometer readings must be corrected when urine contains high glucose or protein, because these substances disproportionately increase the refractive index, leading to falsely elevated specific gravity (SG) values.

  • Glucose: Each 1 g/dL of glucose adds ~0.004 to the SG.

  • Protein: Each 1 g/dL of protein adds ~0.003 to the SG.

• Corrections involve subtracting these contributions to estimate the true electrolyte-based SG.

Why Not the Others?

• b) Ketones and bilirubin: Do not significantly affect refractometry.

• c) Blood and nitrite: May indicate pathology but do not require SG correction.

• d) Urobilinogen and bacteria: Irrelevant to refractometer accuracy.

Modern refractometers are typically temperature-compensated, meaning temperature does not significantly interfere with their readings.

In contrast, glucose, protein, and sodium can elevate refractometer readings because they increase the solute concentration and affect light refraction.

Why the Others Interfere:

• a) Glucose and b) Protein: High levels overestimate true SG because they refract light more than electrolytes (though refractometers are less affected than reagent strips).

• d) Refractometers measure total solute concentration (including electrolytes like Na⁺), and sodium is a normal, expected component of urine. Unlike glucose/protein, Na⁺ does not cause disproportionate refraction artifacts.

Clear, red urine (i.e., red in color but not cloudy) typically indicates the presence of hemoglobin or myoglobin, as both are pigmented proteins that dissolve in urine and give it a red color without turbidity. In contrast, RBCs usually cause cloudy or hazy red urine.

Why Not the Others?

• c) Bacteria – Do not cause red urine unless there is concurrent bleeding (e.g., hemorrhagic cystitis).

• d) Uric acid – At high concentrations, uric acid can cause orange or pinkish sediment, but not clear red urine.

• Urine that develops a “port wine” or dark red/brown color after air exposure is classic for acute intermittent porphyria (AIP), where porphobilinogen (a heme precursor) oxidizes into porphyrins upon standing.

• This is a pathognomonic sign of porphyria and occurs due to light-sensitive porphyrin derivatives.

Why Not the Others?

• a) Melanin: Causes black urine (e.g., metastatic melanoma), not port wine.

• c) Bilirubin: Turns urine dark amber/foamy (liver disease), but doesn’t change after air exposure.

• d) Urobilinogen: Oxidizes to urobilin (yellow-brown), not red.

Key Points:

• Diagnostic tests:

  • Watson-Schwartz test: Detects porphobilinogen in urine.

  • UV light: Porphyrins fluoresce pink-red.

• Clinical correlation: Abdominal pain, neuropsychiatric symptoms.

• Turbid, milky urine caused by chyle (lymphatic fluid rich in fats) is termed chyluria. This occurs due to lymphatic obstruction (e.g., filariasis, trauma, or tumors), which forces chyle into the urinary tract.

• Filariasis (parasitic infection by Wuchereria bancrofti) is the most common global cause, disrupting lymphatic drainage.

Why Not the Others?

• a) Nephrotic syndrome: Causes foamy urine (proteinuria) but not milky turbidity.

• b) Pyuria: Leads to cloudy urine from WBCs (e.g., UTI), but not a milky appearance.

• d) Proteinuria: Does not cause turbidity; frothiness is typical.

• High urine specific gravity (SG >1.030) indicates concentrated urine, commonly caused by:

  • Diabetes mellitus: Excess glucose in urine (glycosuria) increases solute concentration, raising SG.

  • Dehydration: The kidneys conserve water, leading to concentrated urine with high SG.

  • Syndrome of inappropriate ADH secretion (SIADH): Excessive water retention concentrates urine.

Why Not the Others?

• a) Renal failure: Typically causes isosthenuria (fixed SG ~1.010) due to loss of tubular concentrating ability.

• b) Diabetes insipidus: Results in very low SG (<1.005) due to dilute urine from impaired water reabsorption.

• c) Overhydration: Leads to low SG (<1.010) as the kidneys excrete excess water.

• Hematuria (presence of red blood cells in urine) is a primary cause of red or pink urine. The color can range from:

  • Light pink (few RBCs) to bright red (gross hematuria, e.g., from UTIs, kidney stones, or trauma).

  • Dark red/brown (if RBCs lyse in acidic urine, releasing hemoglobin).

Why Not the Others?

• a) Diabetes mellitus: Causes polyuria (frequent urination) but not red urine unless complicated by hemorrhagic cystitis.

• c) Proteinuria: Leads to foamy urine, not discoloration.

• d) Hypersthenuria (high specific gravity): Indicates concentrated urine (dark yellow), not red/pink.

Key Points:

• Dipstick + Microscopy: Confirms hematuria (RBCs on microscopy).

• False red urine:

  • Foods (beets, berries).

  • Drugs (rifampin, phenazopyridine).

  • Hemoglobinuria/myoglobinuria (no RBCs on microscopy).

• Cloudy urine is most commonly caused by bacteria and white blood cells (WBCs), which indicate a urinary tract infection (UTI). The cloudiness results from pus (pyuria) and bacterial growth.

• Other possible causes include crystals, mucus, or epithelial cells, but infection is the most clinically significant.

Why Not the Others?

• a) Uric acid – Can cause pink-orange crystals but usually doesn’t make urine uniformly cloudy.

• b) Mucus – May cause mild cloudiness, especially in normal vaginal or urethral secretions, but is less concerning than infection.

• d) Ketones – Do not cause cloudiness; they are invisible and detected only by dipstick.

• Glucose in urine (glycosuria) does not cause cloudiness. It is a soluble substance that remains invisible in urine, even at high concentrations (e.g., uncontrolled diabetes mellitus).

Why the Others Cause Cloudiness:

• a) WBCs (Pyuria): White blood cells (e.g., from UTIs) make urine cloudy or purulent.

• b) Bacteria: Bacterial growth (e.g., E. coli) causes turbidity due to microbial proliferation.

• c) Mucus: Common in normal urine, especially in women, causing mild haze.

Key Points:

• Cloudy urine is typically due to:

  • Infection (WBCs, bacteria).

  • Crystals (phosphates, urates).

  • Contaminants (mucus, semen, vaginal discharge).

• Glucose is detected by dipstick, not visual inspection.

• Foamy urine is most commonly caused by proteinuria, particularly albumin, which reduces surface tension and creates persistent foam (like soap bubbles). This is a classic sign of nephrotic syndrome or other glomerular diseases.

Why Not the Others?

• a) Ketones: Do not cause foaming (urine may smell fruity but remains clear).

• b) Bilirubin: Causes yellow-brown, foamy urine in liver disease, but foam is less prominent than with heavy proteinuria.

• d) Crystals: Cause cloudiness, not foam.

• A “mousy” or “musty” odor in an infant’s urine is a classic clinical sign of phenylketonuria (PKU), an inherited metabolic disorder caused by a deficiency of the enzyme phenylalanine hydroxylase (PAH). This leads to the accumulation of phenylalanine and its byproducts, including phenylpyruvic acid, which is excreted in urine and produces the distinctive odor 123.

Why Not the Others?

• b) Acetone: Causes a fruity/sweet odor (e.g., diabetic ketoacidosis).

• c) Coliform bacteria: Typically produce a foul or ammonia-like smell (UTIs).

• d) Porphyrin derivatives: Associated with maple syrup urine disease (sweet odor) or porphyria (varied odors, not mousy).

Key Points:

• PKU diagnosis:

  • Newborn screening (Guthrie test or tandem mass spectrometry) detects elevated phenylalanine 29.

  • Urine ferric chloride test: Turns green in the presence of phenylpyruvic acid 9.

• Treatment: Lifelong low-phenylalanine diet to prevent intellectual disability and neurological damage

• Amorphous phosphates are a common cause of cloudy urine and form in alkaline urine (pH >7.0). These crystals precipitate when urine becomes overly basic, often due to:

  • Dietary factors: High intake of dairy (calcium) or citrus fruits (citrate) .

  • UTIs with urea-splitting bacteria (e.g., Proteus), which raise urine pH.

  • Metabolic conditions like renal tubular acidosis (type 1) or prolonged antacid use

Why Not the Others?

• a) Acidic pH: Favors uric acid or calcium oxalate crystals, not phosphates .

• c) High specific gravity: Concentrated urine can promote crystallization but is not specific to phosphates .

• d) Proteinuria: Causes foamy urine, not cloudiness from crystals .

Key Points:

• Clinical significance: Amorphous phosphates are usually benign but may indicate alkaline urine or UTI .

• Differentiation: Unlike pyuria (WBCs causing cloudiness), phosphate cloudiness dissolves with acetic acid

• A fixed specific gravity (SG) of 1.010 (isosthenuria) indicates that the kidneys cannot concentrate or dilute urine properly, a hallmark of chronic renal disease. This occurs due to:

  • Tubular dysfunction: Damaged nephrons lose the ability to reabsorb water/solutes.

  • Loss of medullary gradient: Essential for urine concentration.

Why Not the Others?

• a) Dehydration: Causes high SG (>1.030) as kidneys conserve water.

• b) Diabetes mellitus: Leads to variable SG (often high due to glycosuria).

• d) UTI: May cause pyuria but does not fix SG.

Key Points:

• Isosthenuria reflects end-stage renal damage, seen in:

  • Chronic glomerulonephritis.

  • Diabetic nephropathy.

• Confirm with labs: Elevated creatinine, low GFR.