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PHYSICAL PROPERTIES Color and clarity pH Specific volume Protein Glucose Etc

Clinical Pathology 3-6: Urinalysis Dr. Arnel Amata December 05, 2011

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YELLOW – urochrome affected by: o Concentration o Food o Dyes o Blood

o Inc salt o Renal shut down o Obstruction to flow ANURIA

NORMAL VOLUME: 700-2000 ml/24 hrs POLYURIA: o Inc fluid intake o Diuretics o Nervousness/anxiety OLIGURIA: o Dec fluid intake or excess fluid loss

FIXED: isosthenuria o Loss of both concentrating and diluting function VOLUME

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NORMAL is clear/transparent ALKALINE: cloudy (precipitation of crystals) UTI: WBC & alkalinity Amorphous urates AMMONIACAL: old specimen FRUITY: ketones FOUL: urinary tract infection ODOR: Volatile Acids

NORMAL: 4 – 8 (usually 6) REAGENT STRIPS USE 2 ACID-BASE INDICATORS: o Methyl red o Bromthymol blue Regulation of blood pH ACID URINE: o High protein diet o Acidosis/uncontrolled DM ALKALINE URINE: o After meals – alkaline tide o High vegetable diets o UTI o Renal tubular acidosis GLUCOSE


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Degree of concentration NORMAL: 1.003- 1.030, usually 1.010 – 1.025 URINOMETER: weighted bulb o Floats “HIGH” in conc spec; “LOW” in dilute o Calibrate to read 1.000 in distilled water o Correct for protein or glucose REFRACTOMETER o Ratio of velocity of light in air to velocity through solution o Correlate well with SPEC GRAVITY

ENZYMATIC TESTS: specific for glucose COPPER REDUCTION TESTS: all reducing sugars o “PASSING THROUGH”: solution goes through entire range of colors and back to “greenish” because of large amounts of sugar


GLUCOSE: glucosuria or glycosuria o Blood levels of glucose exceed renal threshold (160 mg/dL)  RENAL GLUCOSURIA  DIABETES MELLITUS – also increased volume with high specific gravity as an attempt to rid blood of excess glucose NON-GLUCOSE REDUCING SUGARS: o LACTOSE: lactating women o GALACTOSE: “galactosemia”, leading to severe mental and physical deterioration and death o FRUCTOSE: sometimes in hepatic disorders o PENTOSES: inherited benign condition KETONES

LOW: hyposthenuria o Diabetes insipidus: impaired ADH o Loss of concentrating ability HIGH: hypersthenuria o Adrenal insufficiency o Hepatic disease o Congestive heart failure


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Cheenee. ANDREW. Shan. FAYE. Ronalie. Amelie. Jr. Pam. Jernell. Dexter. Rubi. Ernie. Gwen. Marcus. AIRA. Noime. Majo. Gecai. Aubrey. Allan. Jeriz. Jay. Rev. Kat. Janel. POUCH. Abi. Gene. Davie. ISSHI. Jacq. Jill. Renz. Barsy. RUTH. Shao. Cristine

Inadeq carbohydrate diet or defect in carbohydrate metabolism Increased fat metabolism, formation of ketone bodies (acetone, acetoacetic acid, β-hydroxybutyric acid) Diabetes mellitus, anorexia, starvation Children more prone to ketosis and ketonuria Not normally detected

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Health UROBILINOGEN BILIRUBIN • • 3 KETONE BODIES: all present in same relative concentration ROTHERA’S TEST: nitroprusside + acetone or acetoacetic acid Normal below detection limit of routine tests COLORIMETRIC METHOD: “protein error of indicators” PRECIPITATION METHODS: sulfosalicylic acid PROTEIN Normal Negative Hemolytic Anemias increase Negative Hepatic disease Neg Pos increase or Biliary obstruction decrease Positive o o o Urobilinogen inc when inc production of bilirubin or when liver doesn’t remove reabsorbed urobilinogen from circulation Urobilinogen dec when normal amounts of bilirubin not excreted into intestinal tract Normally a small amount of urobilinogen in urine DIPSTICK METHOD • • • PROTEINURIA OR ALBUMINURIA: DETECTABLE LEVELS OF PROTEIN IN URINE • • • • • In health.5 – 4 gm/day o Most renal disorders MINIMAL: < 0. removed from albumin. remainder globulin In renal d/o. water insoluble o In liver.5 gm/day o Renal tubule disorders or lower urinary tract POSTURAL PROTEINURIA BLOOD DEGREES OF PROTEINURIA MICROSCOPIC EXAM: – RBCs – WBCs – Epithelial cells – Crystals – Cast • • • • • • • • • 0-3/hpf “ghost cells” Crenated in conc urine Hemolyzed in dilute urine Dysmorphic rbc’s RBCs DYSMORPHIC RBC • • • • HEMOGLOBIN catalyzes oxidation of TETRAMETHYLBENZIDINE with peroxide to yield a blue color May be intact red cells (hematuria) or free hemoglobin (hemoglobinuria) Hemoglobinuria o Traumatic passage thru urinary tract o Dilute urine o Transfusion reaction Hematuria o Renal disorders o Neoplasm o Trauma BILIRUBIN & UROBILINOGEN • EARLY SIGNS OF HEPATOCELLULAR DISEASE o Bilirubin formed from breakdown of Hb in reticuloendothelial cells of spleen and bone marrow o Linked to albumin and carried to liver – INDIRECT OR UNCONJUGATED BILIRUBIN. 60% albumin Most impt indicator of renal disease Amount of protein depends on nature of disorder and to lesser extent severity of disease May be intermittent or continuous MARKED: > 4 gm/day o Nephrotic syndrome o Severe glomerulonephritis MODERATE: 0. conjugated with glucuronic acid – DIRECT. 1/3 albumin. CONJUGATED or water soluble o Conjugated bilirubin excreted in bile and enters intestinal tract o Conjugated bilirubin converted to urobilinogen by intestinal microflora o 50% of urobilinogen is reabsorbed and re-excreted by liver (small amount in urine) and 50% excreted through feces o Bilirubinuria in any d/o that inc conjug bilirubin in blood stream  LIVER DISEASES: hepatocytes can’t excrete all bilirubin into bile  Obstructive biliary tract • • • 0-3/hpf Pyuria “glitter cells” in dilute specimens WHITE BLOOD CELLS .

White cell c. GRANULAR o coarse or fine 3. FATTY o break down of tubular epithelium containing fat oval bodies – DEGENERATIVE TUBULAR DISEASE . Epithelial cell 2. ACID Triple phosphate CRYSTALS ACID TO SL ALKALINE Calcium oxalate ALKALINE Calcium carbonate Ammonium biurate CELLULAR .RED CELL ACID URINE Amorphous urates Uric acid ALKALINE TO SL.WHITE CELL (below) Calcium oxalate crystals WAXY Triple phosphates (toblerone-like accdg. Red cell b. Amata) • • CASTS PRECIPITATION OF PROTEIN – takes on shape of renal tubules formation requires: o Acid pH o Dr. CELLULAR a.• • • Squamous Transitional Renal tubular cells EPITHELIAL CELLS CELLULAR . WAXY o final degeneration of granular – CHRONIC RENAL FAILURE 4. Urine o Decreased urinary flow o Protein FATTY – OVAL FAT BODIES TYPES OF CASTS: 1.