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Common Laboratory Tests

Author: akil, Posted on Sunday, September 05 @ 22:43:17 IST by RxPG  

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This chapter discusses the normal and pathologic values for commonly ordered tests of the blood (cells and chemistries), urine, cerebrospinal fluid, and other serous fluids. The tests discussed here are those in common use for helping to formulate physiologic and diagnostic hypotheses. There are many more tests used in the diagnosis of a specific disease. These tests are highly specific, but may not be sensitive. They are a useful means for confirming an hypothesis, but should not be used until a narrow differential diagnosis has been established. These more specific tests are not discussed here.

Laboratory tests are ordered by the clinician for one of four reasons:

1. Screening: A small number of tests have been demonstrated to find "silent" disease in the patient who has no symptoms or signs or specific risk factors for the disease. Common examples include testing for hemochromatosis with iron studies and for hypercholesterolemia.

2. Case finding: Some tests are used to find disease in specific clinical populations at risk, even if signs or symptoms are not present. They differ from screening tests because they are not used in the general population. An example is testing the bone density of elderly women for osteoporosis.

3. Diagnosis: This is the use of tests to assist in making (or excluding) a diagnosis suggested by the symptoms and signs in patients.

4. Monitoring: Tests are often used to monitor the progress of disease, response to therapy, or concentration of medication.

Blood Chemistries

ALKALINE PHOSPHATASE, SERUM. Pathophysiology: This includes a number of cellular enzymes that hydrolyze phosphate esters. They are named from their optimum activity in alkaline media. High concentrations of the enzymes occur in the blood during periods of rapid growth, either physiologic or pathologic, and from cellular injury. The enzymes are normally plentiful in hepatic parenchyma, osteoblasts, intestinal mucosa, placental cells, and renal epithelium. Abnormally rapid growth or cell destruction will augment the blood concentration of these enzymes.

Normal Alkaline Phosphatase: 30-120 U/L (SI Units: 0.5-2.0 nkat/L). It is high in newborns, declining until puberty and then rising every decade after 60 years of age.

Increased Alkaline Phosphatase. This is usually associated with disorders of bone, liver or the biliary tract. CLINICAL OCCURRENCE: Technical Error dehydration of blood specimen; Endocrine hyperparathyroidism (osteitis fibrosa cystica), acromegaly, hyperthyroidism (effect on bone), subacute thyroiditis, last half of pregnancy; Idiopathic Paget disease, benign transient hyperphosphatasemia; Infectious liver infections (hepatitis, abscesses, parasitic infestations and infectious mononucleosis), chronic osteomyelitis; Inflammatory/Immune primary biliary cirrhosis, sarcoidosis; Mechanical/Trauma healing fractures, common bile duct obstruction from stone or carcinoma, intrahepatic cholestasis, passive congestion of the liver; Metabolic/Toxic osteomalacia, rickets, drug reactions (intrahepatic cholestasis), chlorpropamide, ergosterol, sometimes intravenous injection of albumin, pernicious anemia, hyperphosphatasia, dehydration, rapid loss of weight; Neoplastic osteoblastic bone tumors, metastatic carcinoma in bone, myeloma, liver metastases, cholangiocarcinoma; Neurologic cerebral damage; Psychosocial abuse with skeletal trauma; Vascular myocardial, renal, and sometimes pulmonary infarction.

Decreased Alkaline Phosphatase. CLINICAL OCCURRENCE: Technical Errors use of oxalate in blood collection; Endocrine hypothyroidism; Idiopathic osteoporosis; Inflammatory/Immune celiac disease; Metabolic/Toxic vitamin D toxicity, scurvy (vitamin C deficiency), milk-alkali syndrome, pernicious anemia/B12 deficiency.

ANION GAP, SERUM. Pathophysiology: The anion gap is the difference between the concentrations of measured cations and the measured anions in the blood, measured in milliequivalents per liter, mEq/L: AG = [Na+] - ([Cl-] + [HCO3-]). The anion gap accounts for phosphates, sulfates, amino acids, and albumin.

Normal Anion Gap: 12 ± 2.

Increased Anion Gap. An increased anion gap indicates the accumulation of organic acids and the presence of an anion gap metabolic acidosis. CLINICAL OCCURRENCE: Ketoacidosis (diabetes, alcoholism, starvation), intoxication with salicylates, methanol or ethylene glycol, lactic acidosis, or renal failure.

Decreased Anion Gap. This occurs uncommonly and suggests the accumulation of positively charged proteins in the blood. CLINICAL OCCURRENCE: Multiple myeloma.

ALANINE AMINOTRANSFERASE, SERUM: ALT. Pathophysiology: This enzyme occurs mostly in hepatocytes with smaller quantities in skeletal and heart muscle. It is released into the circulation when cells are damaged or necrotic.

Normal Concentration: 0-35 U/L (SI units: 0-0.58 mkat/L).

Increased ALT. Increased ALT usually indicates damage to the liver, although severe damage to skeletal muscle can produce significant elevations. CLINICAL OCCURRENCE: Infectious viral hepatitis, infectious mononucleosis, liver abscess; Mechanical/Trauma passive liver congestion, extrahepatic biliary obstruction; Metabolic/Toxic drug-induced liver disease, alcohol; Neoplastic hepatocellular carcinoma, liver metastases.

ASPARTATE AMINOTRANSFERASE, SERUM: AST. Pathophysiology: This enzyme is concentrated mostly in the cells of the heart, liver, muscle, and kidney; lesser amounts are in pancreas, spleen, lung, brain, and erythrocytes. Tissue injury releases the enzyme into the extracellular fluids, but not necessarily in amounts proportionate to the injury.

Normal AST: 9-40 U/L.

Increased AST. This usually reflects damage to the liver, the muscles, including the heart, and, less commonly, to other organs. It usually rises in concert with the ALT. When the AST is ≥2.0 times the ALT, alcohol abuse with cirrhosis or alcoholic hepatitis should be suspected. CLINICAL OCCURRENCE: Technical Error false-positive from opiates and erythromycin, dehydration of blood specimen; Congenital muscular dystrophy; Endocrine diabetes mellitus; Idiopathic Paget disease, cholecystitis; Infectious viral hepatitis, pulmonary infections; Inflammatory/Immune hemolytic diseases, polymyositis, pancreatitis, regional ileitis, ulcerative colitis; Mechanical/Trauma severe exercise, clonic and tonic seizures, crushing or burning or necrosis of muscle, inflammation from intramuscular injections, rhabdomyolysis, peptic ulcer, extrahepatic biliary obstruction; Metabolic/Toxic hepatic necrosis and drug-induced hepatitis, uremia, myoglobinemia, pernicious anemia, drugs (salicylates, alcohol), dehydration; Neoplastic bone metastasis, myeloma; Neurologic; Psychosocial; Vascular myocardial, renal and cerebral infarction.

Decreased AST. CLINICAL OCCURRENCE: Endocrine pregnancy; Metabolic/Toxic chronic dialysis, uremia, pyridoxine deficiency, ketoacidosis, beriberi, severe liver disease.

BICARBONATE, TOTAL SERUM (HCO3-, CO2 CONTENT). Pathophysiology: Bicarbonate (HCO3-) is formed in the kidney by carbonic anhydrase and diffused through the body fluids as ionized bicarbonate in association with sodium. Bicarbonate is the major buffer consumed when protons (H+) are produced by the metabolism of amino acids or the increased production or ingestion of organic acids. It accumulates to buffer the acidosis of hypoventilation (increased PaCO2). In respiratory alkalosis with a low PaCO2, the kidney excretes bicarbonate to maintain the blood pH and the bicarbonate concentration falls.

Normal Serum Bicarbonate: 22-26 mEq/L (SI: 22-26 mmol/L).

Increased Bicarbonate. This indicates a metabolic alkalosis, either primary or secondary to a respiratory acidosis. CLINICAL OCCURRENCE: Endocrine hyperaldosteronism, Cushing disease, severe hypothyroidism; Metabolic/Toxic primary metabolic alkalosis (diarrhea, gastric suction, nausea, and vomiting), diuretics (especially loop diuretics), hypercapnia; Psychosocial bulimia, purging.

Decreased Bicarbonate. A decreased bicarbonate concentration indicates the presence of a metabolic acidosis. These are further classified by the anion gap, see page 935. CLINICAL OCCURRENCE: Endocrine Addison disease; Metabolic/Toxic hypocapnia from hyperventilation, metabolic acidosis, for example, renal failure, ketoacidosis (diabetic, alcoholic, starvation), lactic acidosis, salicylate intoxication, methanol or ethylene glycol intoxication, renal tubular acidosis.

BILIRUBIN, TOTAL SERUM. Pathophysiology: See Jaundice, page 539. Unconjugated bilirubin is insoluble in water until conjugated in the liver with glucuronic acid. Four-fifths or more is derived from the catabolism of the heme from aging erythrocytes. The water-soluble conjugated bilirubin is normally excreted in the bile. It is bound to the plasma proteins; when the level exceeds 0.4 mg/dL, the water-soluble form appears in the urine.

Normal Serum Bilirubin: 0.3-1.0 mg/dL (SI Units: 5.1-17 mmol/L).

Increased Bilirubin: Hyperbilirubinemia. Increased bilirubin indicates an increased breakdown of red blood cells or failure of hepatic excretion. CLINICAL OCCURRENCE: Congenital Dubin-Johnson disease, Gilbert syndrome; Idiopathic acute cholecystitis; Infectious viral hepatitis, infectious mononucleosis; Inflammatory/ Immune hemolysis; Mechanical/Trauma common bile duct obstruction, hemolysis; Metabolic/Toxic drug-induced hepatitis, alcoholic hepatitis, cirrhosis, or any cause; Vascular pulmonary infarction, gastrointestinal bleeding, hematoma.

Unconjugated Hyperbilirubinemia. This is caused by hemolysis, ineffective erythropoiesis, decreased hepatic uptake of unconjugated bilirubin (Gilbert syndrome), or impaired hepatic conjugation (neonatal jaundice, drugs or Crigler-Najjar syndrome).

Conjugated Hyperbilirubinemia. Because the liver is able to conjugate bilirubin, the problem is either hepatocyte excretion (Dubin-Johnson syndrome, Rotor syndrome), intrahepatic cholestasis (hepatitis, drugs, granulomatous disease), or bile duct obstruction.

Decreased Bilirubin: Hypobilirubinemia. Nonhemolytic anemias and hypoalbuminemia.

BLOOD UREA NITROGEN, SERUM: BUN. Pathophysiology: Molecular weight 60. Urea is synthesized in the liver from ammonia derived from the metabolism of protein in the body and gut. It is filtered and reabsorbed by the kidney; reabsorption is inversely related to the rate of urine flow.

Normal Serum Blood Urea Nitrogen (BUN): 10-20mg/dL (SI Units: 3.6-7.1 mmol/L).

Increased BUN. An increase indicates decreased glomerular filtration and/or increased tubular reabsorption, or increased production in the gut from ingested protein or blood. CLINICAL OCCURRENCE: Prerenal hypotension, hemorrhage, dehydration (vomiting, diarrhea, excessive sweating), Addison disease, hyperthyroidism, heart failure, sepsis, upper gastrointestinal hemorrhage, increased protein ingestion; Renal any cause of acute or chronic renal insufficiency; Postrenal obstruction of the ureters, bladder, or urethra.

Decreased BUN. CLINICAL OCCURRENCE: Low-protein diets, muscle wasting, starvation, cirrhosis, cachexia, high urine flow.

BUN:Creatinine Ratio Greater than 10:1. This indicates relatively preserved glomerular filtration with either increased urea production or decreased urine flow. CLINICAL OCCURRENCE: Excessive protein intake, blood in the gut, excessive tissue destruction (cachexia, burns, fever, corticosteroid therapy); postrenal obstruction, inadequate renal circulation (heart failure, dehydration, shock).

BUN:Creatinine Ratio Less than 10:1. This indicates decreased urea production. CLINICAL OCCURRENCE: Low protein intake, multiple dialyses, severe diarrhea or vomiting, hepatic insufficiency.

B-TYPE NATRURETIC PEPTIDE. Pathophysiology: Heart failure is accompanied by increased wall tension in the ventricles and atria because of dilation. Natruretic peptides types A and B are released into the circulation in congestive heart failure.

Normal Concentration: 400 ng/dL, often >1000 ng/dL), inflammation, infection, or cancer.

Decreased Serum Ferritin. CLINICAL OCCURRENCE: Iron deficiency.

GLUCOSE, SERUM. Pathophysiology: This is a six-carbon monosaccharide, a primary energy source for metabolism. The serum level remains fairly constant during fasting; there is a moderate rise after the ingestion of food. Hepatocytes convert other carbohydrates to glucose. Surpluses of glucose are converted to glycogen in the liver and muscle, or form fat that is deposited throughout the body, predominately in adipocytes. Glucose uptake by the liver, muscle, and adipocytes is insulin dependent. After an average meal, the normal person has a blood sugar rise to approximately 180 mg/dL serum; this returns to normal fasting levels within 2 hours. Higher blood glucose levels result from excessively rapid absorption or impaired peripheral disposition, usually related to insulin insufficiency or resistance. When the blood concentration of glucose becomes high, the tubular reabsorption threshold is exceeded and glucose is excreted in the urine (glycosuria). The normal renal threshold occurs at a serum glucose of 160-190 mg/dL. This may be higher in a damaged kidney.

Normal Serum Glucose: 75-110 mg/dL (SI Units: 4.2-6.4 mmol/L).

Diagnostic Criteria for Diabetes.

1. A fasting glucose of ≥126 mg/dL (SI Units: ≥7.0 mmol/L); or

2. Symptoms of diabetes plus a random glucose of ≥200 mg/dL (SI Units: ≥11.1 mmol/dL); or

3. A plasma glucose ≥200 mg/dL (SI Units: ≥11.1 mmol/L) 2 hours following a 75-g oral glucose load.

The abnormal test must be confirmed on another day.

Diagnostic of Impaired Fasting Glucose (IFG). A fasting glucose of 110-126 mg/dL (SI Units: 6.1-7.0 mmol/L).

Diagnostic of Impaired Glucose Tolerance (GT). A blood glucose of 140-199 mg/dL (SI Units: 7.8-11.0 mmol/L) 2 hours after a 75-g oral glucose load.

Increased Glucose: Hyperglycemia. Hyperglycemia indicates insulin resistance from the metabolic syndrome, diabetes or release of stress-associated hormones (epinephrine, cortisol, growth hormone). CLINICAL OCCURRENCE: Endocrine diabetes mellitus, impaired glucose tolerance, acromegaly, hyperthyroidism, Cushing disease, increased adrenalin, adrenocorticotropic hormone (ACTH), pheochromocytoma, pregnancy, toxemia of pregnancy; Infectious any acute severe infection, for example, pneumonia; Inflammatory/Immune systemic inflammatory response syndrome (SIRS), regional enteritis, ulcerative colitis; Metabolic/Toxic drugs (corticosteroids, diazoxide, epinephrine), poisoning (streptozotocin); Neurologic Wernicke syndrome, subarachnoid hemorrhage, hypothalamic lesions, convulsions; Vascular myocardial infarction, pulmonary embolism, hemorrhage.

Decreased Glucose: Hypoglycemia. Inability to maintain a normal blood glucose indicates excessive insulin secretion or administration, or severely impaired hepatic gluconeogenesis. CLINICAL OCCURRENCE: Congenital galactosuria, maple syrup urine disease, hepatic glycogenoses; Endocrine hypopituitarism, hypothalamic lesions, hypothyroidism, Addison disease; Infectious sepsis; Inflammatory/Immune pancreatitis; Mechanical/Trauma postgastrectomy dumping syndrome, gastroenterostomy; Metabolic/Toxic insulin administration, oral hypoglycemics, glycogen deficiency, hepatitis, cirrhosis, malnutrition; Neoplastic insulinoma, some sarcomas.

HEMOGLOBIN A1C: GLYCOHEMOGLOBIN. Pathophysiology: Glycosylation of cellular and extracellular proteins occurs at a rate dependent upon the ambient plasma glucose concentration. Hemoglobin is glycosylated in this manner and the amount of glycosylated hemoglobin is an accurate measure of the average blood sugar over the average life of the circulating erythrocytes, approximately 6 weeks. Measurement of one glycosylated form of hemoglobin, hemoglobin A1c, is used to estimate the average blood sugar as a determinate of diabetes control.

Normal Hemoglobin A1c: 3.8-6.4% (SI Units: 0.038-0.064).

IRON, SERUM (FE2+). Pathophysiology: The body contains about 3-4 g of iron. It is a component of hemoglobin, the cytochromes, and other cellular metalloproteins. Approximately 1 mg of iron is absorbed and excreted each day. Most of the iron circulates in erythrocyte hemoglobin (1.0 mg/1.0 mL packed erythrocytes), with the rest bound to ferritin in stores (approximately 1.0 g), in myoglobin, and with a small fraction incorporated into respiratory enzymes and other sites. Iron is absorbed in the duodenum by a complex pathway regulated at the level of the enterocyte; most ingested iron is not absorbed, or is sloughed in the enterocytes, never entering the plasma. Absorbed iron is bound to transferrin. Iron is cleared from the plasma with a half-time of 60-120 minutes, and 80-90% is incorporated into new circulating erythrocytes over the subsequent 2 weeks. The serum concentration of iron decreases by 50-100 ug/dL with the diurnal acceleration of erythropoiesis in the afternoon, so the time of day the specimen is drawn and its relationship to meals should be known. Iron deficiency is a very common disorder.

Normal Serum Iron: 50-100 mg/dL (SI Units: 9-27 mmol/L).

Increased Serum Iron: Hyperferremia. An increase in serum iron may be seen following a high-iron meal, or with hemochromatosis and liver disease. CLINICAL OCCURRENCE: Congenital hemochromatosis, thalassemia; Inflammatory/Immune acute hepatic necrosis, aplastic anemia, hemolytic anemia; Metabolic/Toxic excessive absorption (iron therapy, dietary excess), cirrhosis, pernicious anemia.

Decreased Serum Iron: Hypoferremia. Low serum iron results from inadequate dietary intake, excessive blood loss (both with increased iron-binding capacity), or chronic inflammation (decreased iron-binding capacity). CLINICAL OCCURRENCE: Endocrine iron loss to the fetus during gestation; Infectious tuberculosis, osteomyelitis, hookworm; Inflammatory/Immune celiac disease, rheumatoid arthritis, systemic lupus erythematosus (SLE); Mechanical/ Trauma intravascular hemolysis with hemoglobinuria (paroxysmal nocturnal hemoglobinuria, march hemoglobinuria, prosthetic heart valves); Metabolic/Toxic iron deficiency, repeated phlebotomy, diminished absorption (decreased ingestion, celiac disease, pica, postgastrectomy); Neoplastic gastrointestinal cancers, loss of transferrin in nephrotic syndrome; Psychosocial poverty; Vascular intrapulmonary hemorrhage (e.g., idiopathic pulmonary hemosiderosis), chronic bleeding (e.g., menorrhagia, hematuria, peptic ulcer disease, gastritis, polyps, ulcerative colitis, colon carcinoma).

IRON-BINDING CAPACITY (TIBC), SERUM TOTAL. The TIBC mainly reflects transferrin and, with the serum iron, helps to distinguish iron deficiency anemias from the anemia of chronic inflammation.

Normal Iron-Binding Capacity: 250-370 mg/dL (SI Units: 45-66 mmol/L).

Increased Iron-Binding Capacity. This generally reflects a response to iron deficiency. CLINICAL OCCURRENCE: Iron deficiency, acute or chronic blood loss, hepatitis, late pregnancy.

Decreased Iron-Binding Capacity. Transferrin falls with chronic inflammation. CLINICAL OCCURRENCE: Anemias of chronic disorders (infections, inflammations, and cancer), thalassemia, cirrhosis, nephrotic syndrome.

LACTIC DEHYDROGENASE (LDH), SERUM. Pathophysiology: This enzyme catalyzes the oxidation of lactate to pyruvate reversibly. It is found in all tissues, so an elevation of the blood level is a nonspecific indicator of tissue damage.

Normal LDH: 100-190 U/L (SI Units: 1.7-3.2 mkat/L).

Increased LDH. Elevations of LDH suggest injury to the muscles, liver, hemolysis, or rapid cell division as in lymphomas. CLINICAL OCCURRENCE: Congenital muscular dystrophy in 10% of cases, progressive muscular dystrophy, myotonic dystrophy (but creatine phosphokinase [CPK] is more specific for muscle than LDH); Endocrine hypothyroidism; Infectious hepatitis with jaundice, infectious mononucleosis; Inflammatory/Immune polymyositis in 25% of cases, dermatomyositis, hemolytic anemias; Mechanical/Trauma cardiovascular surgery, common bile duct obstruction, intestinal obstruction; Metabolic/Toxic muscle necrosis, celiac disease, untreated pernicious anemia, alcohol; Neoplastic 50% of cases of lymphoma and leukemia; Vascular acute myocardial infarction, pulmonary embolism or infarction.

Decreased LDH. CLINICAL OCCURRENCE: Irradiation, ingestion of clofibrate.

PHOSPHATE, SERUM INORGANIC. Pathophysiology: This term includes the inorganic phosphorus of ionized HPO42- and H2PO4 in equilibrium in the serum; only 10-20% is protein bound. Phosphorus is necessary for synthesizing nucleotides, phospholipids, and the high-energy adenosine triphosphate (ATP). Phosphates are excreted by the kidney; parathormone (PTH) increases phosphate excretion. When the energy demands are great for glycolysis, the serum inorganic P is decreased.

Normal Phosphate: 3.0-4.5 mg/dL (SI Units: 1.0-1.4 mmol/L).

Increased Phosphate: Hyperphosphatemia. CLINICAL OCCURRENCE: Congenital Fanconi disease; Endocrine acromegaly, hyperparathyroidism; Idiopathic Paget disease; Infectious sepsis; Inflammatory/Immune sarcoidosis; Mechanical/Trauma healing fractures, crush injury, high intestinal obstruction; Metabolic/Toxic acute and chronic renal failure, vitamin D deficiency (rickets, osteomalacia), muscle necrosis, milk-alkali syndrome, respiratory alkalosis, excess of vitamin D; Neoplastic multiple myelomas, osteolytic metastases, myelocytic leukemia.

Decreased Phosphate: Hypophosphatemia. CLINICAL OCCURRENCE: Congenital primary hypophosphatemia; Endocrine hyperparathyroidism, diabetes mellitus; Metabolic/Toxic renal tubular defects (Fanconi syndrome), anorexia, vomiting, diarrhea, lack of vitamin D, in refeeding after starvation, malnutrition, gout, ketoacidosis, respiratory alkalosis, hypokalemia, hypomagnesemia, primary hypophosphatemia, drugs (intravenous glucose, anabolic steroids, androgens, epinephrine, glucagon, insulin, salicylates, phosphorus-binding antacids, diuretic drugs, alcohol).

POTASSIUM, SERUM (K+). Pathophysiology: This is the predominant cation in the intracellular fluid, while sodium predominates in the extracellular fluids. Approximately 90% of the exchangeable K+ is within the cells; less than 1% is in the normal serum. Small shifts of K+ from the cells causes relatively large changes in the smaller serum [K+]. Intracellular acidosis causes an extracellular shift of K+. Plasma [K+] is tightly regulated by the kidney; hyperkalemia leads to aldosterone secretion and potassium excretion. Changes in serum concentration of K+ produce profound effects on nerve excitation, muscle contraction, and in cardiac conduction. Because the concentration of K+ in the erythrocytes is about 18 times as great as that in the serum, hemolysis occurring during sample collection falsely elevates the serum K+.

Normal Potassium: 3.5-5.0 mEq/L (SI Units: 3.5-5.0 mmol/L).

Increased Potassium: Hyperkalemia. (Note: high levels of serum K+ pose great danger of producing cardiac arrest.) CLINICAL OCCURRENCE: Technical Error hemolysis in performing venipuncture or intentional clotting in collecting blood specimens, especially with thrombocytosis; Congenital hyperkalemic periodic paralysis; Endocrine primary and secondary hypoaldosteronism, adrenal insufficiency (Addison disease, adrenal hemorrhage); Mechanical/Trauma rhabdomyolysis, crush injury, hemolyzed transfused blood, urinary obstruction; Metabolic/Toxic acute and chronic renal failure, acidosis (metabolic or respiratory), muscle necrosis, drugs (amiloride, spironolactone, triamterene, angiotensin-converting enzyme inhibitors), foods (fruit juices, soft drinks, oranges, peaches, bananas, tomatoes, high-protein diet), dehydration; Neurologic status epilepticus; Vascular gastrointestinal hemorrhage, hemorrhage into tissues.

Decreased Potassium: Hypokalemia. This is almost always associated with depletion of in total body K+. CLINICAL OCCURRENCE: Endocrine diabetes mellitus, Cushing syndrome, hyperaldosteronism; Mechanical/Trauma ureterosigmoidostomy with urinary reabsorption, adynamic ileus; Metabolic/Toxic vomiting, gastric suction, postgastrectomy dumping syndrome, gastric atony, laxative abuse, polyuria, renal injury, salt-losing nephritis, metabolic alkalosis (from diuresis, primary aldosteronism, pseudoaldosteronism), metabolic acidosis (from renal tubular acidosis, diuresis phase of tubular necrosis, chronic pyelonephritis, diuresis after release of urinary obstruction), malabsorption and malnutrition, drugs (diuretics, estrogens, salicylates, corticosteroids) Neoplastic aldosteronoma, villous adenoma, colonic cancer, Zollinger-Ellison syndrome.

PROTEIN, TOTAL SERUM. Pathophysiology: Most serum proteins are synthesized in the liver (albumin and others) or by mature plasma cells (immunoglobulins). Increases or decreases in serum proteins represent a balance between synthesis and protein catabolism or loss into third spaces or in the urine. This is the total of the serum albumin and the serum globulins; the fibrinogen was discarded in the clot that separated from the plasma to form the serum specimen. The quantity of the total serum protein, minus the albumin fraction, gives an estimate of the serum globulins.

Normal Total Protein: 5.5-8.0 g/dL (SI Units: 55-80 g/L).

Increased Total Protein: Hyperproteinemia. This represents increased concentration of normal proteins, or excessive production of immunoglobulins. CLINICAL OCCURRENCE: Water depletion, multiple myeloma, macroglobulinemia, and sarcoidosis.

Decreased Total Protein: Hypoproteinemia. This is caused by decreased synthesis, increased catabolism because of malnutrition, or loss into third spaces or into the urine in nephrotic syndrome. CLINICAL OCCURRENCE: Congestive cardiac failure, ulcerative colitis, nephrotic syndrome, chronic glomerulonephritis, cirrhosis, viral hepatitis, burns, malnutrition.

PROTEIN: ALBUMIN, SERUM. Pathophysiology: Molecular weight about 65,000. Normally, albumin comprises more than half the total serum protein. Because its molecular weight is low compared to that of the globulins (between 44,000 and 435,000), its smaller molecules exert 80% of osmotic pressure of the plasma. In addition, (a) serum albumin serves as a protein store for the body that can be used when a deficit develops; (b) it serves as a solvent for fatty acids and bile salts; and (c) it serves as a transport vehicle by loosely binding hormones, amino acids, drugs, and metals.

Normal Albumin: 3.5-5.5 g/dL (SI Units: 35-55 g/L).

Increased Albumin: Hyperalbuminemia. No significant correlation with diseases.

Decreased Albumin: Hypoalbuminemia. CLINICAL OCCURRENCE: Congenital analbuminemia; Endocrine diabetes mellitus; Infectious viral hepatitis; Inflammatory/Immune ulcerative colitis, protein-losing enteropathies, chronic glomerulonephritis, lupus erythematosus, polyarteritis, rheumatoid arthritis, rheumatic fever; Mechanical/Trauma peptic ulcer; Metabolic/Toxic congestive cardiac failure, cirrhosis, nephrotic syndrome, malnutrition, drugs (estrogens); Neoplastic multiple myeloma, Hodgkin disease, lymphocytic leukemia, macroglobulinemia.

PROTEIN: GLOBULINS, SERUM. The difference between the values for total serum protein and for serum albumin is referred to as the serum globulin fraction of the serum protein. When the globulin level is increased, fractionation of the globulins is indicated to identify each component. This is accomplished by serum protein electrophoresis.

SERUM PROTEIN ELECTROPHORESIS (SPEP). The proteins are separated by electrophoresis; the proteins migrate, each at its own rate, dependent on its charge and molecular weight. A serum specimen contains proteins that separate into several zones according to their mobility. The proteins are named for the zone in which they are found (named with Greek lowercase letters): alpha 0 (for albumin), alpha 1 (α1), alpha 2 (α2), beta (β), gamma (γ), and phi (φ) (for fibrinogen).

PROTEIN: ALPHA-1 (α1)-GLOBULINS. Alpha-1-globulins include α1-antitrypsin, oromucil, and some cortisol-binding globulin.

Increased a1-Globulins. Hodgkin disease, peptic ulcer, ulcerative colitis, cirrhosis, metastatic carcinoma, protein-losing enteropathy.

Decreased a1-Globulins. Viral hepatitis.

PROTEIN: ALPHA-2 (α2)-GLOBULINS. Alpha-2- globulins include macroglobulins, haptoglobin, HS glycoprotein, ceruloplasmin, and some immunoglobulins.

Increased a2-Globulins. Hodgkin disease, peptic ulcer, ulcerative colitis, cirrhosis, nephrotic syndrome, chronic glomerulonephritis, systemic lupus erythematosus, polyarteritis nodosa, rheumatoid arthritis, metastatic carcinoma, protein-losing enteropathies.

Decreased a2-Globulins. Cirrhosis, viral hepatitis.

PROTEIN: BETA (β)-GLOBULINS. Beta-globulins include transferrin, hemopexin, and some immunoglobulins.

Increased b-Globulins. Rheumatoid arthritis, rheumatic fever, analbuminemia.

Decreased b-Globulins. Nephrotic syndrome, lymphocytic leukemia, metastatic carcinoma.

PROTEIN: GAMMA (γ)-GLOBULINS. Gamma globulins are predominately immunoglobulins of the IgG class. Increases in gamma globulins can be (a) monoclonal, arising from a clonal proliferation of plasma cells or lymphocytes, or (b) polyclonal, as part of an inflammatory response. Polyclonal gamma globulins produce a broad-based pattern in the gamma zone, indicating the presence of proteins from many cell lines.

Increased Polyclonal g-Globulins. Cirrhosis, myelocytic leukemia, lupus erythematosus, rheumatoid arthritis, analbuminemia.

Decreased Polyclonal γ-Globulins. Nephrotic syndrome, lymphocytic leukemia, common variable immunodeficiency, hypogammaglobulinemia, protein-losing enteropathies.

PROTEIN: IMMUNOGLOBULIN IgG. Pathophysiology: Molecular weight 160,000. This is the smallest molecule of the immunoglobulins and the only one that can pass the placental membrane; consequently, it serves as a protection for the newborn until the child's own immunoglobulins can be generated. IgG is synthesized after IgM in response to a new antigen. IgG producing plasma cells are the major humoral effector of chronic inflammation.

Normal IgG: 800-1500 mg/dL (SI Units: 8.0-15.00 g/L).

Increased IgG. CLINICAL OCCURRENCE: Infectious pulmonary tuberculosis, hepatitis, osteomyelitis; Inflammatory/Immune systemic lupus erythematosus, rheumatoid arthritis, vasculitis; Metabolic/Toxic cirrhosis; Neoplastic myeloma, monoclonal gammopathy of undetermined significance (MGUS).

Decreased IgG. CLINICAL OCCURRENCE: Congenital lymphoid aplasia, agammaglobulinemia; Inflammatory/Immune common variable immunodeficiency, nephrotic syndrome; Neoplastic heavy- chain disease, IgA myeloma, macroglobulinemia, chronic lymphocytic leukemia.

PROTEIN: IMMUNOGLOBULIN IgA. Pathophysiology: Molecular weight 170,000. This globulin is especially involved in the protection against viral infections. It has an excretory form with a molecular weight of 400,000, found in colostrum, saliva, tears, bronchial secretions, gastrointestinal secretions, and nasal discharges. It has a special action against viruses of influenza, poliomyelitis, adenoviral diseases, and rhinoviruses.

Normal IgA: 90-325 mg/dL (SI Units: 0.90-3.2 g/L).

Increased IgA. CLINICAL OCCURRENCE: Congenital Wiskott-Aldrich syndrome; Inflammatory/Immune systemic lupus erythematosus, rheumatoid arthritis, sarcoidosis; Metabolic/Toxic cirrhosis; Neoplastic IgA myeloma.

Decreased IgA. CLINICAL OCCURRENCE: Congenital absent in some people, hereditary telangiectasia, lymphoid aplasia; Inflammatory/Immune nephrotic syndrome, Still disease, systemic lupus erythematosus, common variable immunodeficiency, agammaglobulinemia; Metabolic/Toxic cirrhosis; Neoplastic heavy-chain disease, acute lymphocytic leukemia, chronic lymphocytic leukemia, chronic myelocytic leukemia.

PROTEIN: IMMUNOGLOBULIN IgM. Pathophysiology: Molecular weight 900,000. This is the largest of the immunoglobulins. It is formed during a primary antibody response. The rheumatoid factor and the isoantibodies anti-A and anti-B belong mostly to this class.

Normal IgM: 45-150 mg/dL (SI Units: 0.45-1.5 g/L).

Increased IgM. CLINICAL OCCURRENCE: Infectious hepatitis, trypanosomiasis; Inflammatory/Immune biliary cirrhosis, rheumatoid arthritis, systemic lupus erythematosus; Neoplastic macroglobulinemia.

PROTEIN: IMMUNOGLOBULIN IgD. Pathophysiology: Molecular weight 185,000. There is no known specific activity for this protein.

Normal IgD: 0-8 mg/dL (SI Units: 0-0.08 g/L).

Increased IgD. Chronic infections, IgD myeloma.

PROTEIN: IMMUNOGLOBULIN IgE. Pathophysiology: Molecular weight 200,000. IgE binds to mast cells in body tissue. Specific antigen (allergen) binding to mast cell IgE causes degranulation of the mast cell and an allergic response. This protein is involved in allergic and atopic reactions.

Normal IgE: 3.5 g/d of proteinuria. Glomerulonephritis, diabetes mellitus, systemic lupus erythematosus, renal vein thrombosis, amyloidosis, and other causes of nephrotic syndrome.

GLUCOSE. Pathophysiology: Glucose is normally filtered in the glomerulus and completely reabsorbed, mostly in the proximal tubule. Glucose in randomly collected fresh urine specimens is normally undetectable. When the serum glucose rises above 200 mg/dL, the filtered load will exceed the capacity for tubular reabsorption and glucose will appear in the urine. Dipsticks, impregnated with glucose oxidase and an indicator color, provide a convenient, rapid and semiquantitative estimate for the patient and physician.

Normal Glucose Excretion: 3-25 mg/dL; 50-300 mg/d.

Increased Urine Glucose: Glucosuria. CLINICAL OCCURRENCE: Hyperglycemia in diabetes mellitus; infrequently with renal abnormalities, including acute tubular damage, hereditary renal glycosuria, and proximal tubular dysfunction as in the Fanconi syndrome.

KETONES. Pathophysiology: Ketones are the products of fatty acid metabolism. Increased ketones in the urine indicate that cellular metabolism is dependent upon fatty acids rather than glucose for energy. Progressively diminished glucose utilization in uncontrolled diabetes mellitus leads to lipolysis with increasing plasma and urinary concentrations of acetoacetic acid, beta-hydroxybutyric acid, and ketones.

Increased Urinary Ketones: Ketonuria. CLINICAL OCCURRENCE: Diabetic acidosis, fasting, starvation, alcoholic ketoacidosis, isopropyl alcohol intoxication (the clue is an obtunded patient with normal glucose and acid-base status and urine tests positive for ketones).

URINARY SEDIMENT. Pathophysiology: Normally erythrocytes, leukocytes, hyaline casts, and crystals (urate, phosphate, oxalate) are found in the sediment of a fresh specimen collected after a night's fast.

PROCEDURE FOR EXAMINING THE URINARY SEDIMENT. Centrifuge 10 mL of urine in a conical tube for 5 minutes, decant the supernatant, flick the tube to disperse formed elements in the remaining drop, and place it on a slide under a cover slip to be examined with the high-power objective of a microscope (hpf). Abnormal numbers of cells and casts or any bacteria reveal the presence of disease.

Erythrocytes: Hematuria. Normal: 0-5 red blood cells (RBCs)/hpf. CLINICAL OCCURRENCE: Microscopic hematuria may occur with fever and exercise and many lesions of the urinary tract from the glomerulus to the urethral meatus [Cohen RA, Brown RS. Microscopic Hematuria. NEJM 2003;348:2330-2338]. Causes of gross hematuria include coagulation defects, renal papillary necrosis, renal infarction, sickle cell disease, glomerulonephritis, Goodpasture syndrome, stone or carcinoma of the kidney, hemorrhagic cystitis, stone or carcinoma of the bladder, and prostatitis.

Leukocytes: Pyuria. Normal: 0-10 white blood cells (WBCs)/hpf. CLINICAL OCCURRENCE: In addition to neutrophils excreted into the urine from the same anatomic sites as erythrocytes, leukocytes from vaginal exudates frequently contaminate routine specimens collected from women. When pyuria exceeding 10 WBCs/hpf is present in an uncontaminated specimen, a site of infection or inflammation in the urinary tract or kidney should be sought.

Casts. Occasional hyalin casts, arising from the normal renal tubular secretion of mucoproteins, are seen in fresh concentrated specimens. Finding many broad, fine, or coarse granular casts (composed of serum proteins like albumin, IgG, transferrin, haptoglobin) in urine containing excessive protein indicates renal parenchymal disease. Red cell casts generally indicate glomerular disease with RBCs passing the damaged glomeruli in large quantities. The urine of patients with the nephrotic syndrome, who exhibit glomerular proteinuria and hyperlipoproteinuria, contains fatty casts, casts with doubly refractile fat bodies, and Maltese crosses when examined in polarized light. Red cell casts, containing 10 to 50 distinct erythrocytes and doubly refractile fat bodies, indicate glomerular disease (glomerulonephritis). White cell and/or renal tubular epithelial cell casts are found in the urinary sediment of patients with pyelonephritis, polyarteritis, exudative glomerulonephritis, and renal infarction. Bacteria accompanying white cell casts indicate urinary tract infection. Broad orange or brown hematin casts occur in acute tubular injury and chronic renal failure.

Cerebrospinal Fluid (CSF)

The brain and spinal cord are surrounded by, and suspended in, a clear, colorless fluid. Patients with acute CNS symptoms often require testing of the fluid. Below are found the most commonly ordered tests, their reference ranges, and the more frequent causes of abnormality.

PROTEIN. Normal CSF Protein: 20-50 mg/dL (SI Units: 0.5-2.0 g/L).

Increased CSF Protein. Traumatic tap, infection, hemorrhage, metabolic and demyelinating disorders.

Decreased CSF Protein. Young children, CSF leakage, water intoxication, CSF removal, hyperthyroidism.

GLUCOSE. Normal CSF Glucose: 40-70 mg/dL (SI Units: 2.2-3/9 mmol/L).

Elevated CSF Glucose. Hyperglycemia.

Decreased CSF Glucose. Hypoglycemia, infection (especially bacterial or mycobacterial), meningeal malignancy.

CELL COUNT AND DIFFERENTIAL. Normal CSF Cell Count: Adult, 0-5 mononuclear cells per microliter; neonates, 0-30 mononuclear cells per microliter.

Increased CSF Leukocytes. Mononuclear cells increase in infection of the CNS (viral and early bacterial meningitis, meningoencephalitis, or abscess), neurologic disorders, and hematologic malignancies. Neutrophils increase in bacterial infection, hemorrhage, and meningeal malignancy. Eosinophils increase in shunt, parasitic infection, and allergic reactions.

Serous Body Fluids

Normally, a very small amount of fluid resides in the pleural, pericardial and peritoneal spaces. Any clinically detectable accumulation of fluid (effusion or ascites) in the cavity is caused by a pathologic condition. Effusions should be examined microscopically to determine the distribution (differential count) of cells and to detect malignant cells. Cell counts are useful in peritoneal fluid (below), but are somewhat less helpful in pleural fluid. Increased inflammatory cells have indications similar to those in other locations: Neutrophils (infection, neoplasm, leukemia); lymphocytes (infection, infarction, lymphoma, leukemia, neoplasm, rheumatologic serositis); eosinophils (air in cavity, infection, infarction, neoplasm, rheumatologic disease, congestive heart failure). Microbiologic examination, stains, and culture are indicated in exudates; cytologic examination will identify abnormal/malignant cells. Effusions are generally classified as transudate (low protein) or exudate (high protein).

Transudates. Transudates, commonly bilateral in the pleural cavities, are secondary to heart failure or medical conditions that cause a low serum albumin, for example, cirrhosis or nephrotic syndrome. Clear and pale, straw-colored fluids are usually transudates, and additional information is rarely provided by testing beyond that required to confirm that the fluid is a transudate. The few cells found in transudates are mesothelial cells and mononuclear cells (lymphocytes and monocytes) with very few neutrophils.

Exudates. Exudates are more frequently unilateral in the pleural cavities and secondary to localized disorders such as infection or neoplasm. Exudates can be cloudy from cellular increases (leukocytes), red or pink from hemorrhage (or trauma), green white from purulence, or milky from increased lipid.

PLEURAL EFFUSION. See page 397. Tests frequently useful in pleural effusions include gross appearance, fluid/serum protein ratios (0.5 = exudate), fluid/serum lactate dehydrogenase (LDH) ratios (0.6 = exudate), fluid/serum cholesterol ratio (0.3 = exudate), morphologic exam (hematology and cytology), and pH (1000/mm3 and low glucose suggests empyema). Note: If the protein and LDH ratios are equivocal, the cholesterol ratios may help identify transudate/exudate. Transudates rarely benefit from further testing. Cell counts are rarely useful.

PERITONEAL EFFUSION: ASCITES. See page 542. Tests frequently useful in peritoneal effusion include gross appearance, serum/ascites albumin concentration gradient, cell count and differential, cytology and cultures for bacteria and mycobacteria.

Serum/Ascites Albumin Gradient. Subtracting peritoneal albumin from simultaneously determined serum albumin determines the serum/ascites albumin gradient. Values 1.1 indicate a transudate (portal hypertension caused by cirrhosis, hepatic vein thrombosis, portal vein thrombosis, congestive heart failure). Note: Protein and lactate dehydrogenase (LDH) ratios described above for pleural fluid are not reliable in peritoneal fluid to separate transudates from exudates.

White Blood Cell Counts. Detection of spontaneous bacterial peritonitis in patients with transudative ascites is important. Neutrophil counts of >250/mm3 indicate infection and the need for treatment and long-term prophylaxis. High leukocyte counts (>500/mm3), mostly mononuclear cells, are also seen in malignancy.

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