Free ASCP MLS Exam Practice Questions Mock Test: Part 14 – (Body Fluids)

Cloudy or turbid synovial fluid is most commonly caused by increased white blood cells (WBCs) or crystals, as seen in:

• Crystal-induced arthritis (e.g., gout [monosodium urate crystals] or pseudogout [calcium pyrophosphate crystals]).

• Septic arthritis (infection → high neutrophils).

• Inflammatory arthritis (e.g., rheumatoid arthritis).

Why Not the Others?

• a) Dehydration → Does not directly affect synovial fluid clarity.

• b) Osteoarthritis → Typically clear and viscous (non-inflammatory).

• d) Hemorrhage → Causes bloody fluid (not necessarily turbid unless mixed with inflammation).

Fibrinogen is absent in normal CSF because:

1. It is a high-molecular-weight clotting factor produced in the liver that cannot cross the intact blood-brain barrier (BBB).

2. Its presence in CSF indicates BBB disruption (e.g., trauma, hemorrhage, or inflammation).

Proteins Normally Found in CSF:

• a) Transferrin → Present (including beta-2 transferrin, a CSF-specific isoform).

• b) Transthyretin (prealbumin) → Synthesized by the choroid plexus (10% of CSF protein).

• c) Albumin → The most abundant CSF protein (passively crosses BBB).

Sperm agglutination (clumping of sperm due to antibodies or infection) is best evaluated using a fresh, unstained wet preparation because:

1. Preserves native interactions: Agglutination is visible as sperm sticking head-to-head, tail-to-tail, or mixed.

2. No artifact from stains/fixatives: Staining can distort or dissolve agglutination.

3. Phase-contrast microscopy enhances visibility of agglutination patterns.

Why Not the Others?

• b) Wright stain or d) Papanicolaou stain → Used for morphology, not agglutination (fixation disrupts clumping).

• c) Eosin-nigrosin stain → Assesses viability (live/dead sperm), not agglutination.

To calculate sperm concentration using a Neubauer counting chamber, use the following formula:

Sperm concentration (sperm/mL)=Average count per square×dilution factor×106Volume of square in mL\text{Sperm concentration (sperm/mL)} = \frac{\text{Average count per square} \times \text{dilution factor} \times 10^6}{\text{Volume of square in mL}}Sperm concentration (sperm/mL)=Volume of square in mLAverage count per square×dilution factor×106​

In this case:

• Dilution factor = 1:20

• Average count = 50 sperm in 2 secondary squares
  → So, 25 sperm per square

• Volume of 1 secondary square = 0.0001 mL

Concentration=0.000125×20​=5,000,000 sperm/mL

LE (lupus erythematosus) cells are neutrophils or macrophages that have phagocytized denatured nuclear material (from antinuclear antibodies, ANAs). Their presence is historically associated with:

1. Systemic lupus erythematosus (SLE), though the test is now obsolete due to low sensitivity/specificity.

2. Mechanism:

   • ANAs bind to nuclear antigens, forming immune complexes.

   • These complexes are ingested by phagocytes, creating LE cells.

Why Not the Others?

• a) Tuberculosis → Diagnosed by acid-fast staining/PCR, not LE cells.

• b) Gout → Identified by MSU crystals, not LE cells.

• d) Bacterial infection → LE cells are not seen in infections.

The ΔA450 (delta optical density at 450 nm) test measures bilirubin pigments in amniotic fluid to assess fetal hemolytic disease (e.g., Rh incompatibility).

Why It’s Affected by Light Exposure:

• Bilirubin is photosensitive and degrades when exposed to light, leading to falsely low ΔA450 values.

• This can underestimate the severity of fetal hemolysis, delaying critical interventions like intrauterine transfusions.

Why Other Tests Are Unaffected:

• a) Lamellar body count (fetal lung maturity): Measures surfactant particles (stable in light).

• b) Alpha-fetoprotein (AFP): Detects neural tube defects; unaffected by light.

• d) Foam stability index (FSI): Assesses surfactant function; no light sensitivity.

When counting both sides of a Neubauer hemocytometer:

1. Calculate the average of the two counts to improve accuracy (reduces variability from loading errors).

2. Formula for WBC/μL:

   WBC/μL=Average count per quadrant×Dilution factorVolume per quadrant (μL)WBC/μL=Volume per quadrant (μL)Average count per quadrant×Dilution factor​

   • Undiluted CSF: Dilution factor = 1.

   • Volume per 1 mm² quadrant: 0.1 μL (depth = 0.1 mm).

   • Example:

     Average=100+502=75⇒75×10.1=750 WBC/μLAverage=2100+50​=75⇒0.175×1​=750 WBC/μL

Why Not the Others?

• a) Sum → Incorrect (would double the true count).

• c) Difference → Illogical (no clinical utility).

• d) Reload → Only needed if counts are wildly discrepant (e.g., 100 vs. 0).

Synovial fluid is normally viscous due to the presence of hyaluronic acid, a glycosaminoglycan secreted by synovial cells. This viscosity:

• Provides lubrication for joints.

• Acts as a shock absorber.

• Decreases in inflammatory conditions (e.g., rheumatoid arthritis), making the fluid thinner.

Why Not the Others?

• a) Peritoneal fluid – Normally serous and thin (transudate or exudate).

• c) Cerebrospinal fluid (CSF) – Clear and watery, not viscous.

• d) Pleural fluid – Typically thin and serous unless exudative (e.g., empyema).

A milky appearance in cerebrospinal fluid (CSF) is most characteristic of lipid accumulation, which can occur in:

• Rare conditions like hypertriglyceridemia (extremely high blood lipids leaking into CSF).

• Iatrogenic causes (e.g., introduction of lipid-containing substances during myelography or other procedures).

Why Not the Others?

• b) Protein → High protein (e.g., in Guillain-Barré syndrome or bacterial meningitis) makes CSF yellow (xanthochromic) or turbid, not milky.

• c) Glucose → Does not affect color/clarity (low glucose suggests infection).

• d) Bacteria → Causes cloudiness/purulence (e.g., bacterial meningitis), not a milky appearance.

Methylene blue staining is a vitality test used to assess sperm viability by distinguishing:

• Live sperm (with intact membranes) → Exclude the dye and remain unstained.

• Dead sperm (with damaged membranes) → Take up the dye and appear blue.

Why Not the Others?

• a) pH → Evaluates seminal fluid acidity but does not assess sperm viability.

• c) Fructose test → Checks for seminal vesicle function/obstruction, not sperm health.

• d) Leukocyte count → Detects infection/inflammation (pyospermia), not viability.

Acid phosphatase is the definitive enzyme marker for seminal fluid because:

1. It is abundant in prostatic secretions (100–1,000x higher than in other body fluids).

2. It remains detectable in dried stains (forensic use).

Why Not the Others?

• b) Alkaline phosphatase → Elevated in bone/placenta, not specific to semen.

• c) Lactate dehydrogenase (LDH) → Nonspecific (found in many tissues).

• d) Aspartate aminotransferase (AST) → Liver/muscle marker, irrelevant to semen.

Polarized light microscopy is primarily used to identify crystals in synovial fluid, including:

1. Cholesterol crystals:

   • Appearance: Large, notched plates with strong birefringence.

   • Clinical relevance: Found in chronic inflammatory effusions (e.g., rheumatoid arthritis).

2. Other crystals (also visible under polarized light):

   • Monosodium urate (gout): Needle-shaped, negatively birefringent.

   • Calcium pyrophosphate (pseudogout): Rhomboid, positively birefringent.

Why Not the Others?

• b) Bacteria → Identified by Gram stain/culture, not polarization.

• c) WBCs or d) RBCs → Viewed with brightfield microscopy (no birefringence).

The formation of turbidity and a clot upon adding acetic acid is a definitive positive mucin clot test, which:

1. Confirms the fluid is synovial fluid (only synovial fluid contains enough hyaluronic acid to form this clot).

2. Distinguishes it from blood or other fluids (e.g., saline, plasma), which do not clot with acetic acid.

Why This Matters Clinically:

• Even small/traumatic aspirates (0.1 mL) can be diagnostic.

• The test is specific to synovial fluid because:

  • Hyaluronic acid (the clot-forming molecule) is exclusive to joints.

  • Blood or transudates will not clot this way.

Why Not the Other Options?

• b) Contains RBCs → True but irrelevant (RBCs don’t cause this reaction).

• c) Inappropriate for analysis → Wrong; the clot confirms synovial origin, so analysis (e.g., crystals, culture) is valid.

• d) Needs diluent → Unnecessary; the clot confirms synovial fluid.

Uniformly light pink and hazy CSF in all 3 tubes suggests subarachnoid hemorrhage (SAH) because:

1. Blood is evenly distributed across all tubes (unlike traumatic tap, where blood clears in later tubes).

2. Haziness reflects RBCs and hemoglobin breakdown products (not just fresh blood).

3. Xanthochromia (yellow supernatant after centrifugation) confirms SAH if present.

Why Not the Others?

• a) Traumatic collection → Blood decreases from Tube 1 → Tube 3; supernatant is clear (no xanthochromia).

• b) Multiple sclerosis → CSF is clear (may show oligoclonal bands but no RBCs).

• c) Centrifugation → Would clarify the fluid (unless SAH is present, causing xanthochromia).

A successful vasectomy is confirmed by the absence of sperm in the ejaculate, termed azoospermia.

Key Points:

1. Vasectomy severs/occludes the vas deferens, blocking sperm transport.

2. Post-vasectomy testing requires two consecutive azoospermic samples (typically 3 months apart).

Why Not Other Options?

• a) pH 7.8 → Normal range (7.2–8.0); irrelevant to vasectomy success.

• b) 50% motility → Indicates active sperm (would mean vasectomy failed).

• d) Negative agglutination → Tests for antisperm antibodies; unrelated to sperm presence.

Elevated pleural fluid amylase is most commonly associated with:

1. Pancreatitis (due to transudation of pancreatic enzymes into the pleural space, often left-sided).

2. Esophageal rupture (due to salivary amylase leakage into the mediastinum and pleural cavity).

Why Not the Others?

• a) Tuberculosis → Pleural fluid shows high adenosine deaminase (ADA) and lymphocytes, not elevated amylase.

• c) Rheumatoid arthritis → May cause exudative effusions but no amylase elevation.

• d) Congestive heart failure (CHF) → Transudative effusion with low amylase.

The Ziehl-Neelsen (ZN) stain is the gold standard for detecting acid-fast organisms (e.g., Mycobacterium tuberculosis) in body fluids because:

1. Stains mycolic acid in bacterial cell walls, resisting decolorization by acid-alcohol.

2. Appearance:

   • Acid-fast bacilli (AFB): Bright red against a blue background.

   • Non-acid-fast cells: Blue.

Why Not the Others?

• a) Wright stain → Identifies blood cells (e.g., WBC differential), not bacteria.

• b) Gram stain → Fails to stain Mycobacterium (weakly Gram-positive but “ghost cells”).

• d) Sudan black → Detects lipids (e.g., in leukodystrophies), not bacteria.

The Light’s criteria (most widely used for pleural fluid classification) indicate this is an exudate based on the following:

1. Fluid/serum total protein ratio >0.5 (Here: 0.9)

2. Fluid/serum LDH ratio >0.6 (Here: 0.7)

3. Fluid LDH >2/3 upper limit of serum LDH (Not provided, but the first two criteria suffice).

Supporting Evidence for Exudate:

• Yellow & cloudy → Suggests inflammation/infection.

• High WBC (1550/μL) with neutrophil predominance → Typical of bacterial infection/empyema.

• Low glucose (45 mg/dL) → Common in exudates (e.g., infection, malignancy).

Why Not Other Options?

• a) Chylous → Milky fluid, high triglycerides (not seen here).

• c) Transudate → Clear fluid, low protein/LDH ratios (e.g., heart failure).

• d) Pseudochylous → Milky but cholesterol-rich (chronic inflammation, e.g., TB).

• Oligoclonal bands (OCBs) in CSF (but not serum) are a hallmark of multiple sclerosis, seen in ~90% of MS patients.

• They represent intrathecal IgG production due to chronic CNS inflammation.

Why Not Other Options?

• a) Guillain-Barré syndrome: Diagnosed by clinical features + nerve conduction studies (OCBs are not typical).

• b) Tuberculosis (TB) meningitis: Shows lymphocytic pleocytosis + high protein (OCBs are nonspecific).

• d) Cryptococcal meningitis: Diagnosed by CRAG testing/culture (OCBs are irrelevant).

A black, tarry stool (melena) is strongly suggestive of upper gastrointestinal bleeding (e.g., peptic ulcer, esophageal varices, gastritis). The dark color results from:

• Hemoglobin degradation → As blood passes through the digestive tract, stomach acid and enzymes convert hemoglobin to hematin, which gives stool its black, tarry appearance.

Why Testing for Occult Blood is Critical:

• Confirms GI bleeding (even if not visibly apparent in less severe cases).

• Differentiates melena from other causes of dark stool (e.g., iron supplements, bismuth subsalicylate).

Why Not the Other Options?

• b) Fecal fat → Tests for steatorrhea (fat malabsorption), which causes greasy, foul-smelling stools, not melena.

• c) Trypsin → Assesses pancreatic function (irrelevant in melena).

• d) Excess mucus → Suggests colitis or infection, but mucus alone doesn’t cause black stools.

• The tau isoform of transferrin (also known as asialo-transferrin) is a carbohydrate-deficient form of transferrin that is specifically found in CSF.

• It is used as a diagnostic marker for CSF leakage (e.g., in cases of rhinorrhea or otorrhea) because it is absent in other body fluids like blood, sweat, or nasal secretions.

Why Not the Others?

• b) Sweat – Contains electrolytes and water, not tau-transferrin.

• c) Seminal fluid – Contains proteins like seminogelin but not tau-transferrin.

• d) Amniotic fluid – Contains fetal proteins but not tau-transferrin.

The presence of small, dark, pepper-like granules in synovial fluid is a classic finding in alkaptonuria, a rare inborn error of metabolism.

Synovial Fluid Findings in Alkaptonuria:

• Darkening of fluid upon standing.

• Pepper-like pigmented granules due to deposits of oxidized HGA.

• May eventually lead to degenerative arthritis in weight-bearing joints.

Why the other options are incorrect:

• b) Rheumatoid arthritis
  ✘ Associated with cloudy fluid, high WBCs, and autoantibodies, not dark granules.

• c) Traumatic collection
  ✘ May contain blood, but not pigmented granules.

• d) Hemorrhagic arthritis
  ✘ Blood-stained fluid may be seen, but not pepper-like granules.

Hyaluronate (hyaluronic acid) is the principal mucin in synovial fluid, responsible for:

1. Viscosity and lubrication of joints.

2. Shock absorption during movement.

3. Forming a mucin clot when acetic acid is added (diagnostic test for synovial fluid).

Why Not the Others?

• a) Pepsin → A digestive enzyme (stomach), not found in joints.

• b) Albumin → A plasma protein that passively enters synovial fluid but does not provide viscosity.

• d) Orosomucoid (α1-acid glycoprotein) → An acute-phase protein, not a mucin.

The CSF cell differential shows:

• Neutrophilic predominance (89%) → Classic for acute bacterial meningitis due to rapid, severe inflammation.

• Low lymphocytes (7%) → Rules out viral/fungal/TB meningitis (which typically show lymphocytosis).

• Absent eosinophils → Excludes fungal/parasitic causes (which may trigger eosinophilia).

Why Not the Other Options?

• a) Viral meningitis → Lymphocytic predominance (>80%), not neutrophils.

• b) Fungal meningitis → Lymphocytes + eosinophils (if present), rarely neutrophilic.

• d) Tubercular meningitis → Mixed lymphocytic/monocytic pattern, not neutrophilic.

High lactate dehydrogenase (LDH) in body fluids indicates:

• Cellular damage or turnover (e.g., malignancy, infection, or inflammation).

• Increased membrane permeability (due to inflammation or necrosis).

Clinical Correlations:

1. Pleural fluid:

   • Exudative effusion (LDH >⅔ upper serum limit, per Light’s criteria).

   • Empyema or malignancy (very high LDH).

2. CSF:

   • Bacterial meningitis (LDH >70 U/L suggests bacterial vs. viral).

3. Ascites:

   • Malignancy or infection (e.g., spontaneous bacterial peritonitis).

Why Not the Others?

• a) Normal metabolism → LDH is not elevated in normal states.

• b) Decreased permeability → LDH rises due to increased permeability (e.g., inflammation).

• d) Electrolyte imbalance → LDH reflects cell injury, not electrolyte shifts.

Pleural effusions caused by congestive heart failure (CHF) are typically transudates, which have the following characteristics:

1. Appearance:

   • Clear and pale yellow (straw-colored) due to low cellular and protein content.

   • Exudates, in contrast, may appear cloudy, bloody, or purulent due to infection/inflammation.

2. Cell count:

   • WBCs <1000/μL (mostly lymphocytes and mesothelial cells).

   • (Option a) >1000 WBC/μL is incorrect—this suggests exudate/inflammation.)

3. Biochemical markers (Light’s criteria):

   • Fluid:serum protein ratio <0.5 (Option d) >0.5 is incorrect—this defines exudates).

   • Fluid:serum LDH ratio <0.6 (Option c) >0.6 is incorrect—this indicates exudates).

Oligoclonal banding (OCB) is the gold standard test to detect intrathecal immunoglobulin synthesis, a hallmark of:

• Multiple sclerosis (MS) (>95% of MS patients show OCBs in CSF but not serum).

• Other CNS inflammatory conditions (e.g., neurosyphilis, CNS lupus).

How It Works:

• Electrophoresis separates CSF and serum proteins.

• OCBs appear as ≥2 unique IgG bands in CSF (not matched in serum), indicating CNS-specific antibody production.

Why Not the Others?

• a) CSF glucose → Reflects infection/metabolism (low in bacterial meningitis), not immunoglobulin synthesis.

• b) CSF/serum albumin index → Measures blood-brain barrier integrity, not antibody production.

• d) Lactate dehydrogenase (LDH) → Nonspecific marker of cell damage (e.g., infection, malignancy).

When only 1 mL of CSF is available, the priority is microbiological testing to diagnose life-threatening infections (e.g., bacterial meningitis). Here’s the rationale:

1. Gram stain and culture → Critical first steps to identify bacteria, guide antibiotics, and prevent treatment delays.

   • Even minimal volume (0.5 mL) suffices for culture.

   • Delay risks false-negative results due to bacterial lysis.

2. Why not other tests first?

   • a) Glucose / b) Total protein → Require larger volumes but are less urgent.

   • c) Manual cell count → Helpful but secondary to ruling out infection.

A pleural fluid pH <7.2 is a critical diagnostic marker for complicated parapneumonic effusions or empyema (pus in the pleural space).

Key Features:

1. Low pH (<7.2) + low glucose → Indicates bacterial infection (e.g., S. pneumoniae, anaerobes).

   • Caused by bacterial glycolysis and acidic byproducts.

2. Urgent drainage required to prevent fibrosis/sepsis.

Why Not Other Options?

• a) Malignancy → pH usually >7.3 (unless very advanced).

• b) Pancreatitis → pH variable (often >7.2 unless infected).

• d) Congestive heart failure → Transudate (pH ~7.4-7.5).

Exudative effusions (e.g., due to infection, malignancy, or inflammation) are characterized by:

1. High LDH (pleural fluid/serum ratio >0.6 or fluid LDH >2/3 upper limit of serum LDH).

2. High protein (pleural fluid/serum ratio >0.5).

3. Low serum-ascites albumin gradient (SAAG) <1.1 g/dL (if ascites).

Why Not Other Options?

• a) Low protein concentration → Seen in transudates (e.g., heart failure).

• b) SAAG >1.1 g/dL → Indicates transudate (e.g., portal hypertension).

• d) Clear, straw-colored fluid → Nonspecific; transudates and some exudates can appear this way

Septic arthritis (a medical emergency) typically presents with:

1. Gross appearance: Cloudy/milky/purulent (due to pus).

2. WBC count: >50,000 cells/µL (often >100,000), with >90% neutrophils.

3. Gram stain: Positive in 50–70% of cases (e.g., S. aureus, N. gonorrhoeae).

4. Culture: Gold standard (positive in 70–90%).

Why Not the Others?

• a) Clear, few WBCs → Non-inflammatory (e.g., osteoarthritis).

• c) Yellow, low protein, negative culture → Traumatic or degenerative effusion.

• d) High viscosity, negative Gram stain → Normal or inflammatory (e.g., rheumatoid arthritis).

Low pleural fluid glucose (<60 mg/dL or fluid/serum ratio <0.5) is associated with:

• Rheumatoid pleuritis (due to impaired glucose transport from inflammation).

• Empyema (bacterial infection consuming glucose).

• Malignancy (tumor metabolism).

• Tuberculous pleurisy.

Why Not the Others?

• a) Congestive heart failure (CHF) and b) Cirrhosis → Transudative effusions with normal glucose.

• d) Pulmonary embolism → Typically normal glucose (unless complicated by infection or infarction).

An L/S (lecithin/sphingomyelin) ratio of 2.4 at 34 weeks indicates:

1. Fetal lung maturity:

   • L/S ratio ≥2.0 confirms adequate surfactant production, reducing the risk of respiratory distress syndrome (RDS).

   • Lecithin (surfactant) increases sharply after 32–34 weeks, while sphingomyelin remains stable.

Why Not the Others?

• b) Fetal lung immaturity → L/S ratio <1.5 suggests immaturity (high RDS risk).

• c) Increased RDS risk → Only if L/S ratio <2.0 (or <1.5 in diabetic pregnancies).

• d) Neural tube defects → Diagnosed by amniotic AFP/acetylcholinesterase, unrelated to L/S ratio.

Exudative pleural effusions are defined by Light’s criteria, which include:

1. Pleural fluid protein >3.0 g/dL (or pleural fluid/serum protein ratio >0.5).

2. Pleural fluid LDH >200 U/L (or pleural fluid/serum LDH ratio >0.6).

3. Pleural fluid LDH >⅔ of the upper limit of normal serum LDH.

Why Not the Others?

• a) Glucose >60 mg/dL → Nonspecific; exudates can have low glucose (e.g., infection, rheumatoid effusion).

• b) LDH <200 U/L → Suggests transudate (exudates have high LDH).

• d) SAAG >1.1 g/dL → Indicates portal hypertension (transudate, e.g., cirrhosis, heart failure).

• Radiographic contrast media (e.g., myelogram dyes) can contaminate CSF, giving it an oily or turbid appearance due to their high viscosity and lipid content.

• This is a known artifact in patients who recently underwent spinal imaging (e.g., myelography).

Why Not Other Options?

• a) White blood cells → Cause cloudiness (not oily texture).

• b) Neutral triglycerides → Seen in chylous CSF (rare, milky rather than oily).

• c) Increased total proteins → May cause yellowing (xanthochromia) but not oiliness.

Bacterial meningitis typically causes the following CSF abnormalities:

1. Low glucose (<40 mg/dL or CSF:serum glucose ratio <0.4) – Due to bacterial glycolysis and impaired transport.

2. High protein (>100 mg/dL) – From blood-brain barrier disruption and inflammation.

3. High lactate (>35 mg/dL) – Reflects anaerobic metabolism by bacteria and neutrophils.

Analysis of Samples:

A decreased CSF glucose concentration (hypoglycorrhachia) is a hallmark of bacterial meningitis due to:

• Glycolysis by bacteria (e.g., Streptococcus pneumoniae, Neisseria meningitidis) consuming glucose.

• Increased WBC metabolism (neutrophils further deplete glucose).

Why Not the Others?

• a) Viral meningitis → CSF glucose is normal or slightly reduced (lymphocytes consume less glucose than bacteria/neutrophils).

• b) Normal aging → No effect on CSF glucose.

• d) Multiple sclerosis → CSF glucose remains normal (MS is an autoimmune demyelinating disorder, not infectious).

The findings of cloudy synovial fluid, decreased viscosity, and a positive Gram stain are classic for septic arthritis, a medical emergency caused by bacterial joint infection (e.g., Staphylococcus aureus, Neisseria gonorrhoeae).

Key Features:

1. Cloudy fluid → Due to high WBCs (often >50,000/μL, predominantly neutrophils).

2. Decreased viscosity → Enzymatic breakdown of hyaluronan by bacteria/inflammation.

3. Positive Gram stain → Direct evidence of bacteria (requires immediate antibiotics).

Why Not Other Options?

• a) Osteoarthritis → Clear fluid, normal viscosity, no Gram stain bacteria.

• b) Gout → Cloudy (due to crystals/WBCs) but Gram stain negative.

• d) Pseudogout → Cloudy (CPPD crystals) but no bacteria on Gram stain.

The pathognomonic finding in pseudogout is the presence of calcium pyrophosphate dihydrate (CPPD) crystals in synovial fluid, identified by:

1. Morphology: Rhomboid or rod-shaped, weakly positively birefringent under polarized light.

2. Clinical correlation:

   • Acute pseudogout (knee/wrist involvement).

   • Chondrocalcinosis (cartilage calcification on X-ray).

Why Not the Others?

• b) Cartilage debris → Seen in osteoarthritis/trauma, nonspecific.

• c) MSU crystals → Needle-shaped, negatively birefringent (gout).

• d) Hemosiderin-laden macrophages → Indicates old hemorrhage, not pseudogout.

• Elevated CSF IgG index is a hallmark of multiple sclerosis (MS), reflecting intrathecal IgG synthesis due to chronic CNS inflammation.

• Formula: (CSF IgG / Serum IgG) ÷ (CSF albumin / Serum albumin).

• Interpretation: IgG index >0.7 suggests CNS-specific antibody production (seen in ~90% of MS cases).

Why Not Other Options?

• a) Guillain-Barré syndrome → Peripheral nerve disorder (CSF shows albuminocytologic dissociation, not elevated IgG index).

• c) Viral meningitis → Lymphocytic pleocytosis (IgG index typically normal).

• d) Tuberculosis → High protein/low glucose (IgG index nonspecific).

A chylous effusion is a milky-white fluid caused by lymphatic fluid leakage (often due to thoracic duct damage, malignancy, or trauma). Its key features are:

• High triglyceride levels (≥ 110 mg/dL confirms chylous effusion).

• Presence of chylomicrons (visible on lipoprotein analysis).

• Sterile and odorless (unlike infected or purulent effusions).

Why Not the Others?

• a) Cloudy, pink, and containing bacteria → Suggests empyema or infected effusion, not chylous.

• b) Clear with high glucose → Seen in transudative effusions (e.g., heart failure) or rheumatoid effusions, not chylous.

• d) Bloody fluid with low protein → Indicates hemorrhagic effusion (e.g., trauma, malignancy), not chyle.

The presence of hyaluronate (hyaluronic acid) at 0.4 g/dL is diagnostic of synovial fluid, as this glycosaminoglycan is:

• Unique to synovial fluid (provides viscosity).

• Absent in other body fluids (e.g., CSF, urine, peritoneal fluid).

Supporting Evidence:

1. Protein (3 g/dL):

   • Consistent with synovial fluid (normal range: 1–3 g/dL).

   • Lower than peritoneal fluid (transudate/exudate overlap).

   • Higher than CSF (normal: 15–45 mg/dL).

2. Glucose (80 mg/dL):

   • Normal for synovial fluid (~blood glucose).

3. Lactate (10 mg/dL):

   • Normal (elevated in septic arthritis).

Why Not the Others?

• a) Urine → No hyaluronate; protein is usually <30 mg/dL.

• c) Peritoneal fluid → No hyaluronate; protein varies (transudate <2.5 g/dL, exudate ≥2.5 g/dL).

• d) CSF → No hyaluronate; protein is much lower (mg/dL range).

• Seminal fluid (semen) is the fluid that contains sperm and is directly involved in male fertility. It is produced by the male reproductive system, including the seminal vesicles, prostate gland, and bulbourethral glands.

The other options are not related to fertility:

• a) Pleural fluid → Found in the lungs (respiratory system).

• b) Peritoneal fluid → Found in the abdominal cavity.

• d) Synovial fluid → Found in joints (lubricates them).

• Urobilin is the primary pigment responsible for the normal brown color of feces. It is formed from the breakdown of bilirubin by intestinal bacteria.

Why Not the Other Options?

• a) Uroerythrin → A pink pigment found in urine (not feces).

• b) Urochrome → Gives urine its yellow color (not feces).

• d) Urobilinogen → A colorless precursor converted to urobilin in the intestines (not directly responsible for stool color).

Key Concept:

• Bilirubin → Urobilinogen → Urobilin (oxidized form, causing brown stool).

The Oil red O stain is used to qualitatively assess fecal fat (steatorrhea) to differentiate:

1. Malabsorption (e.g., celiac disease) vs. maldigestion (e.g., pancreatic insufficiency).

2. Method:

   • Slide 1 (ethanol pretreatment): Highlights neutral fats (triglycerides).

   • Slide 2 (acetic acid pretreatment): Reveals split fats (fatty acids/soaps).

3. Results:

   • Neutral fats only → Suggests pancreatic insufficiency (maldigestion).

   • Split fats only → Indicates bile acid deficiency (malabsorption).

   • Both → Mixed etiology.

Why Not the Others?

• a) Safranin → Used for bacterial stains (e.g., spore-forming bacteria).

• c) Eosin-nigrosin → Assesses sperm viability, not fecal fat.

• d) Methylene blue → Stains nuclei/mucin, irrelevant for fat evaluation.

Specific gravity is one of the traditional physical properties used to help differentiate transudates from exudates in pleural fluid:

• Transudates typically have a low specific gravity (<1.016) due to low protein content (e.g., in heart failure, cirrhosis).

• Exudates have a higher specific gravity (>1.016) because of increased protein, cells, or other solutes (e.g., in pneumonia, malignancy).

Why Not the Others?

• b) Color → May suggest hemorrhage (bloody) or infection (purulent), but does not reliably distinguish transudates vs. exudates.

• c) Clarity → Transudates are usually clear, while exudates may be cloudy, but this is subjective and overlaps with other conditions.

• d) Volume → Reflects severity but not the underlying pathophysiology (both transudates and exudates can be large).

• Xanthochromia (yellow or pink discoloration of CSF supernatant) is most commonly caused by subarachnoid hemorrhage (SAH).

• It results from hemoglobin breakdown into bilirubin (takes 12+ hours to develop after bleeding).

Key Points:

1. SAH:

   • Xanthochromia peaks at 48 hours and can persist for 1–4 weeks.

   • Spectrophotometry (measuring ΔA450) is the gold standard for detection.

2. Why Not Other Options?

   • a) Traumatic tap: Causes RBCs in CSF, but supernatant remains clear if centrifuged immediately (no time for hemoglobin breakdown).

   • b) Viral meningitis / d) Encephalitis: May elevate WBCs/protein but do not cause xanthochromia.

An exudative pleural effusion is defined by Light’s criteria, which includes:

1. Pleural fluid/serum protein ratio >0.5

2. Pleural fluid/serum LDH ratio >0.6

3. Pleural fluid LDH > ⅔ of the upper limit of serum LDH

Why Not the Others?

• a) Protein ratio <0.5 → Suggests a transudate (e.g., heart failure, cirrhosis).

• c) Glucose >60 mg/dL → Nonspecific; exudates can have low glucose (e.g., infection, rheumatoid effusion).

• d) Clear appearance → Transudates are typically clear, but exudates can be clear or cloudy.

The CSF/serum albumin index is the most specific and widely used calculation to assess blood-brain barrier (BBB) integrity.

Key Points:

1. Albumin is produced only in the liver and does not cross an intact BBB.

2. The index compares CSF albumin to serum albumin, correcting for plasma leakage.

   • Formula: *(CSF albumin / Serum albumin) × 10³*

3. Interpretation:

   • Normal: <9 (intact BBB)

   • Elevated: ≥9 (BBB dysfunction, e.g., meningitis, MS, or trauma).

Why Not Other Options?

• a) CSF IgG index → Evaluates intrathecal IgG synthesis (MS, infections), not BBB integrity.

• b) Total protein ratio → Less specific (affected by non-albumin proteins).

• d) LDH ratio → Nonspecific marker for cell damage (e.g., infections/hemorrhage).

Rhombic crystals with weak positive birefringence are pathognomonic for calcium pyrophosphate dihydrate (CPPD), the hallmark of pseudogout:

1. Morphology: Rhomboid or rod-shaped.

2. Birefringence:

   • Weakly positive (blue when parallel to the compensator axis).

   • Less intense than monosodium urate (MSU).

3. Clinical correlation:

   • Pseudogout (acute CPP crystal arthritis).

   • Chondrocalcinosis (cartilage calcification on X-ray).

Why Not the Others?

• a) Cholesterol → Notched plates, no consistent birefringence (chronic inflammation).

• b) Hydroxyapatite → Non-birefringent (requires electron microscopy).

• c) Monosodium urate (MSU) → Needle-shaped, strongly negatively birefringent (gout).

A SAAG >1.1 g/dL indicates portal hypertension as the cause of ascites, including:

• Cirrhosis (most common cause).

• Heart failure.

• Budd-Chiari syndrome (hepatic vein obstruction).

Why Not the Others?

• a) Peritoneal carcinomatosis → SAAG <1.1 g/dL (exudative, due to tumor infiltration).

• b) Tuberculosis → SAAG <1.1 g/dL (exudative, from inflammation).

• d) Pancreatic ascites → SAAG variable but typically <1.1 g/dL (due to pancreatic duct leak).

Key Point:

• SAAG formula:

  $$\text{SAAG}=\text{Serum albumin}-\text{Ascitic fluid albumin}$$

• High SAAG (>1.1) = Transudate (portal hypertension).

• Low SAAG (<1.1) = Exudate (infection, malignancy, or pancreatitis).

Decreased CSF total protein concentration is most commonly associated with:

• CSF leakage (e.g., due to trauma or lumbar puncture complications) → Dilution of CSF by extracellular fluid lowers protein levels.

• Conditions causing increased CSF production (e.g., hydrocephalus) → Faster turnover dilutes protein content.

Why Not the Other Options?

• a) Meningitis → Increases CSF protein due to inflammation and blood-brain barrier disruption.

• b) Carcinoma (neoplastic meningitis) → Elevates CSF protein from tumor infiltration.

• c) Hemorrhage (subarachnoid or traumatic) → Raises CSF protein due to blood contamination.

Pilocarpine iontophoresis is the standard method to stimulate sweat production for:

1. Cystic fibrosis (CF) diagnosis: Measures chloride concentration in sweat ([Cl⁻] >60 mmol/L is diagnostic).

2. Autonomic dysfunction evaluation (e.g., small fiber neuropathy).

Procedure:

• Pilocarpine (a cholinergic agonist) is delivered via low electric current to the skin.

• Sweat is collected on filter paper/a coil and analyzed for electrolytes.

Why Not the Others?

• b) Separate CSF proteins → Done by electrophoresis, not iontophoresis.

• c) Measure ions in saliva → Saliva tests use passive collection, not iontophoresis.

• d) Determine serous fluid pH → pH is measured directly (e.g., with a pH meter).

The results are physiologically normal because:

1. CSF glucose is ~60–70% of serum glucose (56 mg/dL CSF vs. 88 mg/dL serum = 64%, within normal range).

2. Whole blood glucose is ~10–15% lower than serum glucose (77 mg/dL vs. 88 mg/dL = 12.5% lower, expected due to RBC water content).

Why Not the Others?

• a) CSF elevated → Incorrect; CSF glucose should be lower than serum.

• b) Whole blood > serum → Never true; whole blood is always lower due to plasma dilution.

• d) Serum = whole blood → Incorrect; they differ predictably (serum lacks RBCs).

Lithium heparin is the preferred anticoagulant for synovial fluid sent for cell count and crystal analysis because:

1. Preserves cell morphology: Unlike EDTA, heparin does not distort WBCs or crystals.

2. No interference with microscopy: Heparin does not form crystals or precipitate (unlike EDTA, which can mimic CPPD crystals).

3. Standard practice: Recommended by the Clinical and Laboratory Standards Institute (CLSI) for synovial fluid analysis.

Why Not the Others?

• a) Liquid EDTA → Can artificially precipitate and mimic calcium pyrophosphate (CPP) crystals, leading to false positives.

• c) Sodium fluoride → Used for glucose preservation (irrelevant for cell counts/crystals).

• d) Sodium polyanethol sulfonate (SPS) → Used for blood cultures (inhibits complement/phagocytosis, unsuitable for synovial fluid).

This scenario describes the Apt test (also called the alkali denaturation test), which is used to distinguish fetal hemoglobin (HbF) from adult (maternal) hemoglobin (HbA) in bloody stools, especially in neonates.

How it works:

• Hemoglobin from the stool sample is extracted into water.

• Sodium hydroxide (NaOH) is added to denature the hemoglobin.

• HbF is resistant to alkali denaturation and remains pink.

• HbA is susceptible to alkali denaturation and turns yellow-brown.

Interpretation in this case:

• The tube turned yellow after adding NaOH → Indicates that the hemoglobin was denatured.

• Therefore, the hemoglobin present was maternal hemoglobin (HbA).

Synovial fluid has two primary physiological roles:

1. Lubrication:

   • Hyaluronic acid and lubricin reduce friction between articular cartilage surfaces during movement.

2. Nutrient delivery:

   • Supplies oxygen and nutrients to avascular cartilage via diffusion.

   • Removes metabolic waste (e.g., CO₂, lactic acid).

Why Not the Others?

• b) Oxygen delivery to muscles → Muscles receive oxygen via blood vessels, not synovial fluid.

• c) Glucose breakdown → Synovial fluid contains glucose but does not metabolize it.

• d) Sodium regulation → Plasma sodium is regulated by kidneys, not joints.

In a healthy individual, CSF glucose is ~60–70% of blood glucose due to:

1. Passive transport across the blood-brain barrier (BBB).

2. Metabolic consumption by CNS cells.

Calculation:

• Blood glucose: 80 mg/dL

• Expected CSF glucose: 80 × 0.6–0.7 = 48–56 mg/dL (closest to 50 mg/dL).

Why Not the Others?

• a) 25 mg/dL → Pathologic (e.g., bacterial meningitis).

• c) 100 mg/dL or d) 150 mg/dL → Higher than blood glucose, which is impossible (CSF glucose never exceeds serum levels).

Creatinine analysis in peritoneal fluid is used to diagnose urine leakage (urinoma) into the peritoneal cavity, which can occur due to:

• Bladder rupture (trauma or iatrogenic injury).

• Urinary tract obstruction (e.g., ureteral tear).

Key Findings:

• Peritoneal fluid creatinine will be markedly higher than serum creatinine (due to concentrated urine).

• Fluid-to-serum creatinine ratio >1.0 confirms urine leakage.

Why Not the Others?

• a) Pericardial fluid → Creatinine is not relevant; suspect uremic pericarditis if BUN/creatinine are high systemically.

• b) Synovial fluid → Creatinine is not measured here (used for crystal analysis or infection).

• c) Pleural fluid → Rarely involved in urine leakage (unless urothorax from obstructive uropathy).

Oligoclonal bands (OCBs) in cerebrospinal fluid (CSF) are immunoglobulin G (IgG) bands detected by electrophoresis that indicate intrathecal antibody production. Their presence is a key diagnostic feature of:

• Multiple sclerosis (MS) → OCBs in CSF but not serum are found in ~90% of MS patients, suggesting CNS-specific immune activity.

• Other neurological conditions (e.g., CNS infections, autoimmune disorders) may also show OCBs, but MS is the most common association.

Why Not the Other Options?

• a) Spina bifida → A neural tube defect, diagnosed via imaging and elevated AFP, not CSF OCBs.

• b) Hydrocephalus → Caused by CSF flow obstruction; diagnosed via imaging, not immunology.

• c) Reye syndrome → A mitochondrial disorder post-viral illness, diagnosed via liver biopsy/metabolic tests, not CSF analysis.

Exudative pericardial effusion is typically caused by inflammatory, infectious, or malignant conditions. The possible causes include:

• Bacterial infection (e.g., tuberculosis, purulent pericarditis) → Leads to an exudative effusion due to inflammation and increased vascular permeability.

• Malignancy (e.g., lung cancer, lymphoma)

• Autoimmune diseases (e.g., lupus, rheumatoid arthritis)

• Radiation therapy

The other options (a, b, d) typically cause transudative effusions:

• Congestive heart failure (↑ hydrostatic pressure)

• Nephrotic syndrome (hypoalbuminemia → ↓ oncotic pressure)

• Cirrhosis (hypoalbuminemia and portal hypertension)

The blood-brain barrier (BBB) tightly controls CSF composition by:

1. Selective permeability:

   • Allows small, lipid-soluble molecules (e.g., O₂, CO₂, ethanol).

   • Blocks large/polar molecules (e.g., proteins, pathogens, most drugs).

2. Cellular transport:

   • Nutrients (e.g., glucose, amino acids) enter via specific transporters.

   • Waste products are actively removed.

Why Not the Others?

• a) Passive diffusion of all substances → Incorrect; the BBB is highly selective.

• b) Prevents water entry → False; water freely crosses via aquaporins.

• d) Facilitates protein entry → False; CSF protein is very low (~15–45 mg/dL) due to BBB exclusion.

Xanthochromia (a yellow or pinkish discoloration of CSF) is most commonly associated with subarachnoid hemorrhage (SAH). It occurs due to the breakdown of hemoglobin into bilirubin (which causes the yellow color) after RBCs lyse in the CSF, typically 12 hours to 2 weeks after bleeding.

Why Not the Others?

• a) Bacterial meningitis → CSF is usually cloudy/turbid (due to high WBCs), not xanthochromic.

• c) Traumatic tap → Fresh blood may be present, but xanthochromia does not appear immediately (centrifugation would show a clear supernatant if it’s just a traumatic tap).

• d) Viral encephalitis → CSF may have mild pleocytosis but remains clear or slightly cloudy, not xanthochromic.

A clot in synovial fluid forms primarily due to the conversion of fibrinogen into fibrin, which occurs when:

• Joint trauma or inflammation allows fibrinogen (a clotting factor from plasma) to leak into the synovial space.

• The synovial fluid, which normally lacks fibrinogen, gains clotting capability when plasma proteins enter.

Why Not the Others?

• a) Inflammatory reaction with increased leukocytes → Causes turbidity but not clotting (unless fibrinogen is also present).

• b) High concentration of mucin (hyaluronic acid) → Increases viscosity, not clotting.

• d) Contamination with blood → Introduces fibrinogen, but clotting is still due to fibrinogen, not blood cells themselves.

The described test—aspirating seminal fluid with a Pasteur pipette and observing droplet formation under gravity—is the standard method to assess semen viscosity:

• Normal viscosity: Forms discrete droplets (not a continuous thread).

• Hyperviscosity: Forms a long, sticky thread (associated with infertility).

Why Not the Others?

• a) Vitality → Requires dye exclusion tests (e.g., eosin-nigrosin) to distinguish live/dead sperm.

• b) Motility → Assessed by microscopic observation of sperm movement (graded as progressive/non-progressive).

• d) Concentration → Measured via hemocytometer or automated counters (counting sperm/mL).

A peritoneal fluid-to-serum amylase ratio >1 strongly suggests pancreatic ascites, caused by:

• Pancreatic duct rupture (e.g., due to chronic pancreatitis or trauma).

• Leakage of pancreatic enzymes (amylase-rich fluid) into the peritoneal cavity.

Key Features:

• Amylase levels in ascitic fluid are markedly elevated (often >1,000 U/L).

• Fluid may appear cloudy or milky (if triglycerides are also high).

Why Not the Others?

• a) Cirrhosis → Ascitic fluid amylase is low (transudative effusion).

• c) Bacterial peritonitis → Amylase is normal or mildly elevated (not ratio >1).

• d) Malignancy → May cause exudative ascites but rarely elevates amylase unless pancreatic tumor.

Normal cerebrospinal fluid (CSF) should appear:

• Clear (free of cloudiness or particles)

• Colorless (like water)

Any deviation from this suggests pathology:

• Cloudiness → Infection (e.g., meningitis) or high cell/protein content

• Pale yellow (xanthochromia) → Subarachnoid hemorrhage (after RBC breakdown)

• Opalescent → Possible lipid or protein abnormality (rare)

Why Not the Other Options?

• b) Opalescent → Abnormal (suggests high lipids or proteins, e.g., metastatic cancer).

• c) Pale yellow → Abnormal (xanthochromia from old blood or hyperbilirubinemia).

• d) Xanthochromic → Always pathological (due to hemoglobin breakdown products).

CEA is the most widely used tumor marker for evaluating malignant effusions because:

1. It is elevated in adenocarcinomas (e.g., lung, colorectal, breast, ovarian).

2. It helps distinguish malignant effusions (high CEA) from benign causes.

Clinical Utility:

• Pleural effusion: High CEA suggests lung or metastatic adenocarcinoma.

• Peritoneal effusion: High CEA may indicate GI (colon, gastric) or ovarian cancer.

• Threshold: CEA >5 ng/mL (serum) or >2.5 ng/mL (effusion) raises suspicion.

Why Not the Others?

• b) JAK2 → Used for myeloproliferative disorders (e.g., polycythemia vera), not effusions.

• c) hCG → Relevant for gestational trophoblastic disease/testicular cancer, rarely in effusions.

• d) CD10 → Marker for renal cell carcinoma/lymphoma, not effusion evaluation.

Pericardial fluid accumulation is normally prevented by lymphatic drainage because:

1. Lymphatic vessels in the parietal pericardium continuously drain fluid, maintaining a balance between production and reabsorption.

2. Normal pericardial fluid volume: 15–50 mL (ultrathin lubricating layer).

Why Not the Others?

• b) High vascular pressure → Incorrect; increased vascular pressure (e.g., heart failure) causes pericardial effusions, not prevention.

• c) Myocardial secretion → False; the myocardium does not secrete fluid.

• d) RBC reabsorption → RBCs play no role in fluid homeostasis.

Birefringence under polarized light occurs when a material splits light into two rays with different refractive indices. Monosodium urate (MSU) crystals exhibit this property because:

1. Crystalline structure: Aligns light predictably, producing bright, needle-shaped crystals.

2. Negative birefringence:

   • Yellow when parallel to the compensator axis.

   • Blue when perpendicular.

3. Clinical correlation: Pathognomonic for gout.

Why Not the Others?

• b) Bacteria → Non-crystalline; no birefringence.

• c) Protein aggregates → Amorphous; no birefringence (e.g., Russell bodies).

• d) Hemoglobin → Non-crystalline; no birefringence (unless converted to heme crystals, which are rare).

The Gram stain is the gold standard for rapid bacterial detection in CSF because:

1. Identifies bacteria by morphology and staining:

   • Gram-positive (e.g., S. pneumoniae, blue/purple).

   • Gram-negative (e.g., N. meningitidis, pink/red).

2. Critical for empiric antibiotic therapy (results within 30 minutes).

Why Not the Others?

• a) Wright-Giemsa → Used for cell differentials (e.g., lymphocytes vs. neutrophils), not bacteria.

• c) Sudan III → Detects lipids (e.g., in demyelination), irrelevant for infection.

• d) Prussian blue → Identifies iron (e.g., hemosiderin in old hemorrhage).

Dark yellow amniotic fluid is most commonly associated with an increased concentration of bilirubin, which occurs in:

• Hemolytic disease of the fetus and newborn (HDFN) (e.g., Rh incompatibility), where fetal RBC breakdown releases bilirubin into the amniotic fluid.

• The ΔOD450 test (spectrophotometric analysis) is used to measure bilirubin levels and assess the severity of fetal hemolysis.

Why Not the Others?

• a) Urea and d) Creatinine → Elevated in fetal renal abnormalities but do not cause yellow discoloration.

• b) Glucose → Does not affect amniotic fluid color (though abnormal levels may indicate maternal diabetes).

Synovial fluid that easily forms small, discrete droplets (instead of a long, viscous string) indicates decreased viscosity, which is most commonly caused by:

• Inflammation (e.g., rheumatoid arthritis, septic arthritis, or crystal-induced arthritis like gout/pseudogout), where inflammatory enzymes break down hyaluronic acid, reducing viscosity.

Why Not the Others?

• a) Gout and b) Pseudogout → Both involve inflammation (due to crystals), leading to low viscosity, but the droplet formation itself is a nonspecific sign of any inflammatory process.

• d) Hypothyroidism → May cause joint stiffness (e.g., hypothyroid arthropathy) but typically does not alter synovial fluid viscosity significantly.

Fixed and stained seminal fluid (with Wright, Giemsa, or Papanicolaou stains) is used to evaluate sperm morphology because:

1. Staining highlights structural details:

   • Head defects (e.g., tapered, vacuolated).

   • Midpiece/tail defects (e.g., coiled, absent).

2. WHO criteria: ≥4% normal forms is considered acceptable (strict thresholds use ≥14%).

Why Not the Others?

• a) Motility → Assessed by fresh, unstained specimen under phase-contrast microscopy.

• b) Viability → Requires dye exclusion tests (e.g., eosin-nigrosin) on live sperm.

• d) Concentration → Measured by hemocytometer/automated counters (unstained).

A milky or turbid appearance in synovial fluid is most commonly caused by crystal-induced arthritis, such as:

• Gout (monosodium urate crystals)

• Pseudogout (calcium pyrophosphate crystals)

Why Not Other Options?

• a) Septic arthritis → Typically purulent (yellow/green, not milky).

• b) Fungal infection → Rare; fluid may be cloudy but not classically milky.

• d) Hemorrhagic effusion → Bloody (red/brown), not milky.

Calcium pyrophosphate dihydrate (CPPD) crystals in compensated polarized light microscopy show:

1. Shape: Rhomboid or rod-shaped.

2. Birefringence: Weakly positive (blue when parallel to the compensator axis, yellow when perpendicular).

3. Clinical correlation:

   • Pseudogout (acute CPP crystal arthritis).

   • Chondrocalcinosis (cartilage calcification on X-ray).

Why Not the Others?

• a) Needle-shaped, yellow → Monosodium urate (gout), which is negatively birefringent.

• c) Hexagonal, colorless → Cystine crystals (seen in cystinosis, not joints).

• d) Round, green → No common crystals match this description.

Eosinophils in CSF (≥10% of WBCs) are rare but strongly suggest:

1. Parasitic infections:

   • Angiostrongylus cantonensis (eosinophilic meningitis).

   • Gnathostoma spinigerum or Baylisascaris procyonis.

2. Other causes (less common):

   • Fungal infections (e.g., Coccidioides).

   • Drug reactions (e.g., NSAIDs, IVIg).

Why Not the Others?

• a) Bacterial meningitis → Neutrophils dominate (eosinophils are rare).

• c) Viral meningitis → Lymphocytes dominate (eosinophils absent).

• d) Traumatic tap → Introduces RBCs, not eosinophils.

Lactate dehydrogenase (LDH) is an enzyme found in cells, and its levels in serous fluids (e.g., pleural, peritoneal, or pericardial fluid) help differentiate between transudates and exudates.

• Increased LDH suggests:

  • Cellular breakdown (due to cell damage or necrosis).

  • Inflammation or infection (e.g., bacterial peritonitis, pleuritis, malignancy).

  • Exudative effusion (as per Light’s criteria, where LDH > 2/3 of the upper limit of serum LDH supports exudate).

Why not the other options?

• a) Transudate:

  • Transudates have low LDH (due to passive fluid leakage without cellular damage, e.g., in heart failure or cirrhosis).

• c) Electrolyte imbalance & d) Dehydration:

  • These do not directly affect LDH levels in serous fluids.

Decreased synovial fluid glucose is most commonly seen in:

• Rheumatoid arthritis (RA) (due to intense inflammation and WBC consumption of glucose).

• Septic arthritis (bacterial infection rapidly consumes glucose).

• Tuberculous arthritis (chronic inflammation).

Why Not the Others?

• a) Osteoarthritis → Normal glucose (non-inflammatory condition).

• b) Gout → Glucose is normal or slightly reduced (crystal-induced inflammation is less glucose-depleting than RA).

• d) Joint trauma → Normal glucose (unless secondarily infected).

• Malignant cells in pleural fluid are diagnostic of carcinomatosis (metastatic cancer involving the pleura).

• Common primary cancers: Lung, breast, lymphoma, ovarian.

Why Not Other Options?

• a) Congestive heart failure → Transudative effusion (no malignant cells).

• b) Liver cirrhosis → Transudative effusion (SAAG >1.1 g/dL).

• d) Tuberculosis → Lymphocytic exudate (malignancy must be ruled out).

Cystic fibrosis (CF) is caused by mutations in the CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) gene, which encodes a chloride channel critical for fluid and electrolyte balance.

• Delta-F508 (ΔF508) is the most common CFTR mutation, accounting for ~70% of CF cases worldwide.

  • This mutation results in a deletion of phenylalanine at position 508, causing protein misfolding and degradation of the CFTR protein.

  • Leads to thick mucus secretions in the lungs, pancreas, and other organs.

Why Not the Other Options?

• a) Fragile X → Causes Fragile X syndrome (intellectual disability), unrelated to CF.

• b) Trisomy 21 → Causes Down syndrome, a chromosomal disorder (extra chromosome 21).

• d) Philadelphia chromosome → Associated with chronic myeloid leukemia (CML), due to BCR-ABL1 fusion gene.

In viral meningitis, CSF glucose is typically:

• Normal (or mildly decreased, but rarely <40 mg/dL).

• This contrasts with bacterial meningitis, where glucose is markedly low (CSF/serum ratio <0.4).

Key CSF Findings in Viral Meningitis:

1. Glucose: Normal (~60-80% of serum glucose).

2. WBCs: Lymphocytic pleocytosis (10–500 cells/μL).

3. Protein: Mildly elevated (50–100 mg/dL).

Why Not Other Options?

• a) Markedly low → Bacterial/TB/fungal meningitis.

• c) Very high → Artifact (e.g., hyperglycemia).

• d) Undetectable → Never occurs in viral meningitis.

CSF lactate levels help differentiate between types of meningitis and neurological conditions:

• Mildly increased lactate (25–30 mg/dL) → Seen in:

  • Fungal meningitis (e.g., Cryptococcus, Candida)

  • Tuberculous meningitis

  • Early or partially treated bacterial meningitis

• Markedly increased lactate (>35 mg/dL) → Classic for acute bacterial meningitis (due to anaerobic glycolysis by bacteria and neutrophils).

Why Not the Other Options?

• b) Multiple sclerosis → Typically has normal lactate (inflammatory demyelination doesn’t increase anaerobic metabolism).

• c) Multiple myeloma → A plasma cell malignancy; CSF lactate is normal unless CNS involvement causes secondary effects.

• d) Bacterial meningitis → Usually causes high lactate (>35 mg/dL); mild elevations are atypical unless treated early.

• Calcium pyrophosphate dihydrate (CPPD) crystals are the hallmark of pseudogout (calcium pyrophosphate deposition disease, or CPPD disease).

• These crystals appear as rhomboid-shaped and are weakly positively birefringent under polarized light.

Why Not Other Options?

• a) Gout → Caused by needle-shaped, negatively birefringent monosodium urate (MSU) crystals.

• b) Rheumatoid arthritis → Inflammatory arthritis without crystals (autoantibodies like RF/anti-CCP are diagnostic).

• d) Septic arthritis → Bacterial infection (e.g., S. aureus); no crystals (unless coincidental CPPD).

Sweat chloride testing is the gold standard diagnostic test for cystic fibrosis (CF), a genetic disorder caused by mutations in the CFTR gene.

• Elevated sweat chloride (>60 mmol/L) → Indicates CF due to defective chloride transport in sweat glands.

• Intermediate levels (30–59 mmol/L) → Require further testing (e.g., genetic analysis).

• Normal levels (<30 mmol/L) → Rule out CF.

Why Not the Other Options?

• a) Multiple sclerosis → A neurological disorder diagnosed via MRI and CSF analysis, unrelated to sweat chloride.

• b) Muscular dystrophy → A muscle-wasting disease diagnosed via genetic testing and muscle biopsy, not sweat tests.

• c) Multiple myeloma → A plasma cell cancer diagnosed via serum protein electrophoresis (SPEP) and bone marrow biopsy, unrelated to sweat electrolytes.

The formation of turbidity and a clot upon adding acetic acid confirms the fluid is synovial fluid, because:

• Hyaluronic acid (unique to synovial fluid) precipitates in acetic acid, forming a mucin clot.

• This reaction does not occur in other body fluids (e.g., blood, saline, or transudates).

Key Observations:

1. Minimal volume (0.1 mL) and slight bloodiness:

   • Suggests a traumatic tap or difficult aspiration, but the mucin clot test overrides this concern.

2. Clot formation:

   • Normal synovial fluid: Forms a tight, ropy clot.

   • Inflammatory fluid (e.g., rheumatoid arthritis): Friable clot.

Why Not the Others?

• b) Contains red blood cells → True but irrelevant (blood doesn’t clot with acetic acid alone).

• c) Is inappropriate for analysis → Incorrect; the clot confirms synovial origin, so analysis is valid.

• d) Must be treated with a diluent → Unnecessary; the clot confirms synovial fluid.

The continuous production and reabsorption of CSF is maintained by:

1. Production:

   • Choroid plexus actively secretes CSF (~20–25 mL/hour) via ion pumps (Na+/K+ ATPase) and selective filtration.

2. Reabsorption:

   • Arachnoid villi/granulations drain CSF into dural venous sinuses via hydrostatic pressure gradients.

Why Not the Others?

• a) Active filtration → Partial truth (choroid plexus uses active transport, but reabsorption is pressure-driven).

• b) Osmotic pressure → Minor role; CSF is isotonic to plasma.

• d) Passive diffusion → Insignificant; CSF production/reabsorption are active processes.

The findings of elevated triglycerides and chylomicrons in milky peritoneal fluid are diagnostic of a chylous effusion.

Key Features of Chylous Fluid:

1. Appearance: Milky/opaque due to high lipid content.

2. Triglycerides: >110 mg/dL (typically much higher in true chylous effusions).

3. Chylomicrons: Present (confirmed by lipoprotein electrophoresis or centrifugation).

4. Causes:

   • Lymphatic disruption (e.g., trauma, surgery, lymphoma, or abdominal malignancy).

   • Congenital lymphatic disorders (e.g., lymphangiectasia).

Why Not Other Options?

• b) Exudate / c) Transudate: These terms describe protein/LDH ratios (Light’s criteria) but do not account for lipid content.

• d) Pseudochylous: Fluid appears milky but has low triglycerides and high cholesterol (seen in chronic inflammation, e.g., tuberculosis or rheumatoid disease).

Malignant cells in serous fluids (pleural, peritoneal, pericardial) typically show:

1. Nuclear atypia:

   • Irregular nuclear membranes (indentations, grooves).

   • Coarse chromatin (clumped or “salt-and-pepper” pattern).

   • Prominent nucleoli.

2. Cytoplasmic features:

   • High nuclear-to-cytoplasmic (N:C) ratio.

   • Vacuolation or signet-ring forms (e.g., gastric adenocarcinoma).

3. Architectural patterns:

   • Cell clusters with loss of polarity (3D groups).

   • Psammoma bodies (in ovarian/thyroid cancer).

Why Not the Others?

• a) Small round cells with uniform nuclei → Benign mesothelial cells or lymphocytes.

• c) Neutrophils in clusters → Suggest infection, not malignancy.

• d) Crystals with birefringence → Seen in gout/pseudogout, unrelated to cancer.

The best way to distinguish a traumatic tap from a subarachnoid hemorrhage (SAH) is by checking for xanthochromia (yellowish discoloration) in the supernatant after centrifugation:

• Traumatic tap (caused by needle injury during LP):

  • Fresh blood mixes with CSF, but no xanthochromia (since RBCs haven’t had time to lyse).

  • Centrifugation yields a clear supernatant (if no prior hemorrhage).

  • RBC count decreases in successive CSF collection tubes.

• Subarachnoid hemorrhage:

  • Xanthochromia is present (due to hemoglobin breakdown into bilirubin, which takes at least 2–12 hours).

  • RBC count remains consistent across all CSF tubes.

Why Not the Others?

• a) Presence of bacteria in Gram stain → Indicates infection (meningitis), not SAH or traumatic tap.

• c) Low glucose concentration → Suggests bacterial meningitis or other infections, not hemorrhage.

• d) Cloudy appearance → Seen in infection (high WBCs) or severe hemorrhage, but not reliable for distinguishing traumatic tap vs. SAH.

Normal adult CSF contains:

1. 0–5 white blood cells (WBCs)/µL, predominantly:

   • Lymphocytes (60–70%).

   • Monocytes (30–40%).

2. Red blood cells (RBCs) should be 0/µL (unless traumatic tap).

Why Not the Others?

• b) 6–15 RBCs/µL → Abnormal (CSF should have no RBCs unless contaminated by blood).

• c) 10–50 neutrophils/µL → Pathologic (suggests bacterial infection or hemorrhage).

• d) 5–10 lymphocytes/µL → Misleading; while lymphocytes dominate, total WBCs should not exceed 5/µL.

Sharp, needle-shaped crystals with strong negative birefringence under polarized light are pathognomonic for monosodium urate (MSU), the hallmark of gout:

1. Optical properties:

   • Negative birefringence: Appear yellow when parallel to the compensator axis.

   • Needle morphology: Often intracellular (within neutrophils during acute attacks).

2. Clinical correlation:

   • Hyperuricemia (though 30% of acute gout occurs with normal uric acid).

   • Podagra (1st MTP joint involvement is classic).

Why Not the Others?

• a) Calcium oxalate → Seen in ethylene glycol poisoning/renal disease, but birefringence is variable (not diagnostic in joints).

• c) Ammonium biurate → Yellow-brown spherules with radial striations (found in urine, not synovial fluid).

• d) Calcium pyrophosphate (CPP) → Rhomboid-shaped, weakly positively birefringent (pseudogout).

The mucin clot test evaluates synovial fluid’s hyaluronic acid integrity by adding 2–5% glacial acetic acid:

• Normal fluid: Forms a tight, ropy clot (intact hyaluronate).

• Inflammatory fluid (e.g., rheumatoid arthritis): Produces a friable, poor clot (hyaluronate degraded by enzymes).

Why Not the Others?

• a) Sodium chloride → Used for crystal analysis (e.g., gout), not mucin clotting.

• b) Hydrochloric acid → No role in synovial fluid testing.

• c) Sodium hydroxide → Used in other lab tests (e.g., protein precipitation) but not for mucin clots.

The string test is the most appropriate and practical method to assess synovial fluid viscosity. It involves:

• Observing the fluid’s ability to form a “string” (4–6 cm long) when dropped from a syringe.

• Normal synovial fluid (rich in hyaluronic acid) is highly viscous and forms a long string.

• Decreased viscosity (e.g., in inflammatory arthritis like rheumatoid arthritis or infection) results in a short or absent string, indicating hyaluronate breakdown.

Why Not the Others?

• b) Refractometry → Measures total protein concentration, not viscosity.

• c) Gram stain → Detects bacteria (used for diagnosing septic arthritis, not assessing viscosity).

• d) Osmometry → Measures osmolality, not viscosity.