Clinical Pathology 3-6 Urinalysis
Clinical Pathology 3-6 Urinalysis
Clinical Pathology 3-6: Urinalysis Dr. Arnel Amata December 05, 2011
CHEMICAL CONSTITUENTS
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
CLARITY
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
pH
CHEMICAL PROPERTIES
SPECIFIC GRAVITY
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
Refractometer
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, -hydroxybutyric acid) Diabetes mellitus, anorexia, starvation Children more prone to ketosis and ketonuria Not normally detected
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3 KETONE BODIES: all present in same relative concentration ROTHERAS 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
increase
or
o o
Urobilinogen inc when inc production of bilirubin or when liver doesnt 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
In health, 1/3 albumin, remainder globulin In renal d/o, 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: 0.5 4 gm/day o Most renal disorders MINIMAL: < 0.5 gm/day o Renal tubule disorders or lower urinary tract POSTURAL PROTEINURIA BLOOD DEGREES OF PROTEINURIA
0-3/hpf ghost cells Crenated in conc urine Hemolyzed in dilute urine Dysmorphic rbcs
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, water insoluble o In liver, removed from albumin, conjugated with glucuronic acid DIRECT, 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 cant excrete all bilirubin into bile Obstructive biliary tract
EPITHELIAL CELLS
ACID URINE Amorphous urates Uric acid ALKALINE TO SL. ACID Triple phosphate
CRYSTALS
WAXY
CASTS PRECIPITATION OF PROTEIN takes on shape of renal tubules formation requires: o Acid pH o Conc. Urine o Decreased urinary flow o Protein
TYPES OF CASTS: 1. CELLULAR a. Red cell b. White cell c. Epithelial cell 2. GRANULAR o coarse or fine 3. WAXY o final degeneration of granular CHRONIC RENAL FAILURE 4. FATTY o break down of tubular epithelium containing fat oval bodies DEGENERATIVE TUBULAR DISEASE