Clinical Lab Test 3 Objectives

1200-1500mL

Oliguria

• Excessive vomiting
• Diarrhea
• Perspiration
• Severe burns

Anuria

• Serious kidney damage
• Decrease in blood flow to kidney

Polyuria (>3 L/day)

• Random
• First morning void
• Midstream clean-catch

First morning void

Fasting (second morning void)

2-hr postprandial

Glucose tolerance test

24-hr urine collection

• Catheterized
• Midstream clean-catch
• Suprapubic aspiration

Suprapubic aspiration

Three-glass collection

Prerenal proteinuria (multiple myeloma)

• Multiple myeloma
• Congestive heart failure
• Renal hypoxia due to renal artery stenosis
• Hypertension
• Fever

Renal proteinuria

• Kidney disease
• Primary/induced glomerular proteinuria
• Tubular proteinuria

• Glomerulonephritis
• Nephrotic Syndrome

• Drugs/toxins
• Systemic disease (diabetes mellitus)

• Defective tubular reabsorption (increased levels of low-molecular weight proteins)
• Caused by acute/chronic pyelonephritis, or drugs/toxins.

Postrenal proteinuria

• Inflammation within the urinary tract, bladder, urethra, prostate gland.
• Contamination with vaginal secretions.

Renal threshold for glucose is exceeded.

170 mg/dL

Indicates excess amounts of circulating intermediary products of fat metabolism in the blood (ketosis), therefore exceeding renal threshold for ketones.

• Cloudy red (urine)
• Normal color (serum)
• Significance: intact RBCs

• Clear red (urine)
• Pink to red (serum)
• Significance: abnormal intravascular hemolysis (hemolytic transfusion reaction, burns, strenuous exercise)

• Clear red-brown
• Normal color (serum)
• Significance: muscle damage (crushing musculoskeletal injuries, rhabdomylosis, MI)

Increased breakdown of Hgb causes increased levels of conjugated bilirubin which cause an increase in urinary urobilinogen and no urinary bilirubin.

Liver is unable to remove reabsorbed urobilinogen from the portal circulation causing increased urinary urobilinogen (or may be absent) and increased urinary bilirubin (varies).

Intra/extra-hepatic obstruction decreases the normal amount of bilirubin being excreted into the intestinal tract, which causes an increase in urinary bilirubin (spills over) and no urinary urobilinogen (decreased).

Indicates presence of bacteria in significant numbers due to infection of the urinary system.

Microscopic examination (urine sediment)

Indicates increased number of WBCs in urine (may be due to infection/inflammation of genitourinary system).

• SG indicates the proportion (ratio) of dissolved solids to the total volume of the specimen (relative degree of concentration).
• Osmolality is a count of the number of particles in a fluid sample (urine/serum).
• (Greater concentration=higher osmolality).

• Indicates bleeding in the urinary tract (without significant proteinuria).
• Caused by urinary tract stones, benign/malignant UT neoplasms, trauma, prostatitis.

Indicates presence of infection/inflammation of the genitourinary system.

Kidney infection

• <5 cells/hpf means "clean" sample
• Most frequently seen and least clinically significant.

• Indicates a poorly collected sample.
• Cannot be sent to micro lab for culture (contaminated).

• Recent instrument procedure (ei, catheterization).
• Suspect a pathologic process if instrument procedure has NOT been performed.

• Necrosis/damage.
• Severe kidney disease exists.

• Oval fat bodies.
• Nephrotic syndrome

Lumen of the distal convoluted tubule and collecting duct.

• Acidic pH: casts dissolve at alkaline pH
• High urine concentration: casts dissolve in dilute urine
• Proteinuria: increased protein level necessary for cast formation
• Stasis: diminished urine flow allows proteins to precipitate in tubules

• Tamm-Horsfall Protein
• Renal tubular epithelial cells

• AMA panel for DM management:
• Basic metabolic panel
• Glycosylated hemoglobin (HbA1C)
• Anion gap
• Lipid profile
• Others to know:
• Ketone bodies
• Microalbumin (early indicator)

HbA1c concentration represents the blood glucose levels over preceding 6-8 weeks.

• Increased in uncontrolled diabetes.
• Results from increased lipolysis and decreased reesterification of FA in to TG, increasing circulating free FAs (ketone bodies).
• Leads to accumulation of acetoacetate and b-hydroxybutyrate in blood (ketoacidosis).

>30, <300 mg/24 hrs of urine albumin excretion (UAE)

• Increase in transcapillary passage of albumin.
• Marker of micro-vascular disease.
• Does NOT indicate smaller than normal sized albumin (greater than normal amount of excretion but less than previously detected levels).

• Sodium
• Potassium
• Calcium
• Magnesium
• Chloride
• Bicarbonate

All metabolic processes are dependent on or affected by electrolytes.

• Water homeostasis
• Acid-base balance (pH regulation)
• Proper heart and muscle function
• Oxidation-reduction reactions
• Enzyme cofactors

• Major cation found in highest concentration in ECF.
• Maintains osmotic pressure and acid-base balance.

• Severe polyuria
• Metabolic acidosis
• Diarrhea
• Addison's disease (rare endocrine disorder)

• Congestive heart failure
• Liver disease (ascites due to osmotic pressure imbalance)
• Renal disease
• Cushing's syndrome

• Major intracellular cation.
• Influences muscle activity of the heart.

• Prolonged diarrhea/vomiting.
• Inadequate intake of dietary potassium.

• Kidney dysfunction
• Urinary obstruction

• Major extracellular anion (along with bicarb).
• Found in serum, plasma, CSF, tissue fluid and urine.
• Key role in maintaining osmotic pressure and electrical neutrality (opposes sodium).

• Congestive heart failure
• Dehydration
• Excessive intake

• Salt loss (NaCl) as seen in chronic pyelonephritis
• Metabolic acidosis (DKA)
• Prolonged vomiting

• Important extracellular anion (along with chloride).
• Is the main form of CO2 in the body, therefore it serves as a measurement of the metabolic component of the acid-base balance.

• Consideration of the other major anions and cations.
• Evaluated using the Anion Gap

A calculation of the mathematical difference between the anions and cations in the body.

Presence of unmeasured anions as seen in metabolic acidosis.

• Uremia (phosphate, sulfate)
• Diabetic ketoacidosis (acetoacetate, beta-hydroxybutyrate)
• Shock
• Exercise-induced physiologic anaerobic glycolysis
• Fructose & phenformin administration (lactate)
• Poisoning by methanol (formate), ethylene glycol (oxalate), salicylates
• Therapy with diuretics, penicillin, carbenicillin

Increase in unmeasured cations which causes an increase in the corresponding measured anion.

• Essential for myocardial contraction.
• Decrease impairs cardiac function, produces irregular muscle spasms.
• Increase results from primary hyperparathyroidism or malignancies.

It is an essential cofactor for >300 enzymes.

• Manifests in cardiovascular and neuromuscular systems.
• Rare in non-hospitalized patients.

• Decreased renal function.
• Intake of magnesium containing medication (antacids).

• Metabolic acidosis/alkalosis
• Respiratory acidosis/alkalosis

Detected by decreased plasma bicarbonate (lost in buffering of excess acid).

• Excess base is added to the system.
• Base elimination is decreased.
• Acid-rich fluids are lost (ei. gastric contents from vomiting).

Decreased elimination of gaseous CO2 which causes increased retention of dissolved CO2.

Increased rate/depth of respiration produces excess elimination of acid via respiratory system.

• HCO3 is low
• pCO2 is low
• Hyperventilation (excretes CO2)

• HCO3 is high
• pCO2 is high
• Hypoventilation (retention of CO2)

• HCO3 is high
• pCO2 is high
• Retention of HCO3 and increased H+ secretion

• HCO3 is low
• pCO2 is low
• Excretion of HCO3 and decreased H+ secretion

• Chief component of NPN (renal function) material in blood.
• Principle waste product of protein degradation.
• Equal in concentration in ICF and ECF.

Uremia

Azotemia

Urea (urea nitrogen/BUN)

Increased protein consumption.

• Degradation product of creatine phosphate in muscle (waste product).
• Produced at a fairly constant rate (readily passed through glomerulus, not reabsorbed).
• Proportional to muscle mass.

• Creatinine clearance
• Measure milliliters of plasma cleared of creatinine by the kidneys in one minute.

• Creatinine production has substantial individual variation.
• Can also be derived from dietary meat (may influence values not associated with muscle mass).
• Many interfering substances may alter results.

• Prediction equations.
• Patients with chronic kidney disease.
• Patients at risk for developing chronic kidney disease.

• Detect onset of renal insufficiency
• Adjust drug dosages for drugs excreted by kidneys
• Evaluate therapies for patient with chronic renal disease
• Document eligibility for Medicare reimbursement (end-stage renal disease)
• Accrue points for patients awaiting kidney transplants

• Essential for structural integrity of cell membranes.
• Component of nucleic acid and high-energy nucleotides (ATP).
• Key role as a buffer to facilitate excretion of H+ (85% exists as HPO4/H2PO4).

• Renal tubular damage
• Non-renal acidosis

• Myoglobin
• Troponin
• CK isoenzyme (CK-MB)

• Heme protein found in muscle.
• Early marker of injured muscle tissue (NOT cardiac specific).
• Elevated levels detectable in 1-3 hours.

• Complex of 3 regulatory proteins present in skeletal and cardiac muscle.
• Is the "gold standard" of cardiac biomarkers (TnI & TnT released into circulation after myocardial tissue damage/more specific for heart injuries than other markers).
• Levels remain elevated for days after MI.

• Found in skeletal muscle, heart muscles, and brain tissue.
• MB (CK-MB) is the most useful marker for evaluating MI.
• Levels increase in 4-6 hours but does not remain elevated as long as troponins.

Natriuretic peptides (B-type (BNP), N-terminal pro B-type (NT-proBNP)).

• Circulating concentrations increase in chronic heart failure.
• Levels of BNP or NT-proBNP in blood relate to the severity of heart failure.
• Higher levels of BNP or NT-proBNP also may be associated with a poor prognosis for the patient.

• It is an acute phase reactant.
• Made by the liver.
• Secreted into the bloodstream within a few hours after the start of an infection or inflammation.

• Increased levels are observed after heart attack, in sepsis, after surgery.
• Can be valuable in monitoring disease activity (level can jump thousand-fold due to inflammation).

No, it is non-specific.

Increased risk for coronary heart disease, stroke, vascular disease.

Folate (B9), B6, or B12 deficiencies.

Potential marker of cardiac disease when there is familial history or lifestyle risk factors.

Metabolizing aspartate and alanine.

• ALT: found primarily in liver and kidney
• AST: found in liver, heart, kidney, pancreas, skeletal muscle

Increases are seen in any condition involving necrosis of hepatocytes, myocardial cells, RBCs or skeletal muscle cells.

• Inflammation of the liver.
• AST usually exceeds ALT

• Hepatic hypoxia (ei. CHF=chronic heart failure)
• Chemical poisoning (ei. Reye's Syndrome)
• Infectious mononucleosis
• Active cirrhosis (ei. from chronic alcohol abuse)

Alanine aminotransferase (ALT)

Serum enzyme levels of ALT/AST are more sensitive to hepatic disease.

• By combining elevations of various liver-associated enzymes into a pattern.
• Typically: increased AST & ALT=liver disease, increased ALP & GGT=biliary disease

• Transfers gamma-glutamyl groups from peptides.
• Present in proximal renal tubule, liver, pancreas and intestine.

• In conditions that cause obstruction of bile ducts.
• It is a very sensitive test for liver damage (alcohol consumption is a common culprit of unexplained/unexpected elevations).

• Present on cell surfaces in most tissues.
• Catalyzes alkaline hydrolyses of many substrates.
• Especially associated with small intestine, bone, liver and placenta.

Bone disorders and liver disease.

• Biliary obstructive disorders; Cholestasis
• Paget's disease of the bone
• Osteomalacia
• Rickets
• Osteogenic sarcoma
• Hyperparathyroidism (disorders involving osteoblasts)

With patterns of clinical findings and other lab tests.

• Main sources are centroacinar cells of the pancreas and salivary glands.
• Catalyzes the breakdown of glycogen and starch.
• Elevated level of activity suggests acute pancreatitis, mumps, parotitis (salivary gland infection).

By releasing digestive enzymes into the plasma and interstitial fluid.

• Found predominantly in the pancreas.
• Hydrolyzes ester linkages of fats to produce alcohols and fatty acids.
• Concentration in the pancreas is 9000 fold greater than any other tissue.

Suggests diagnosis of acute pancreatitis.

• Lipase (LPS) and amylase (AML).
• Lipase is more specific for pancreatic disease.

• LPS remains elevated for up to 7 days.
• AML remains elevated for up to 3 days.
• (After acute inflammatory event).

• Albumin
• Globulin
• Miscellaneous

• Albumin
• Prealbumin

• Alpha-1 globulins
• Alpha-2 globulins
• Beta-globulins
• Gamma-globulins

• Myoglobin
• Troponin

• Alpha-1 antitrypsin (AAT)
• Alpha-1 fetoprotein (alpha fetoprotein, AFP)

• Haptoglobin
• Cerulopasmin
• Alpha-2 macroglobulin

• Transferrin
• Hemopexin
• Complement proteins
• Fibrinogen
• C-Reactive Protein (CRP)

Immunoglobulins A, D, E, G, and M

• Albumin
• Contributes nearly 80% of the colloid osmotic pressure of intravascular fluid (maintains fluid balance in tissues).
• Acts as carrier protein for bilirubin, hormones, fatty acids, drugs, calcium and magnesium.

• Liver disease
• Renal disease
• Malnutrition
• Gastrointestinal loss (inflammation)
• Muscle-wasting diseases

Dehydration

• Carrier protein for thyroid hormones thyroxine (T4) and triiodothyronine (T3).
• Transports vitamin A (complexed w/retinol binding protein).

• Is a sensitive marker of inadequate dietary protein intake.
• Is decreased in hepatic disease, acute inflammatory responses and tissue necrosis.

Neutralizes trypsin-like enzymes (elastase) that can damage structural proteins in surrounding tissue.

Deficiency is associated with severe degenerative emphysematous pulmonary disease.

Protects fetus from "attack" by mother's immune system.

Between 15th and 20th wk of gestation (freely crosses placenta).

• Elevated AFP: suggests possible open neural tube defect, atresia of the GI tract, and/or fetal distress.
• Low AFP: associated with increased risk of Down's syndrome and trisomy 18.

• Liver cancer
• Some adult gonadal cancers

Hepatocytes and cells of the reticuloendothelial (RE) system.

It binds free Hgb.

A copper-containing protein with enzymatic activity.

In ceruloplasmin.

Indicates Wilson's disease (inherited disease where copper is deposited in the liver, brain and skin causing brain and neurologic damage).

Large protein synthesized by hepatocytes found mainly in intravascular spaces.

Inhibits a variety of protease enzymes (trypsin, pepsin, plasmin).

Seen in renal disease.

• Synthesized by liver.
• Major component of the beta-globulin fraction.

• Transport of iron.
• Prevents loss of iron through the kidneys.

• Two
• About 1/3

Seen in liver disease (decreased synthesis).

The liver.

• Removes circulating heme and porphyrins.
• Increased in malignant melanoma (skin cancer).

Complement proteins

• Lysis of cell to which Ag-Ab complexes are attached.
• Opsonization (increases phagocytosis).

• Increased levels: found in inflammatory states.
• Decreased levels: found in systemic lupus erythematosis.

Fibrinogen

Formation of fibrin clot when activated by thrombin (not seen in serum).

• Disseminated Intravascular Coagulation (DIC)
• Afribinogenemia (rare inherited disorder)

C-reactive protein (CRP)

Facilitates complement coating (opsonization) of bacteria, fungi, etc.

• Acute rheumatic fever
• Myocardial infarction
• Viral/bacterial infections
• Rheumatoid arthritis

• Immunoglobulins
• IgG is most abundant

• Plasma cells (B lymphs)
• Stimulated by an immune response to foreign material.

IgA

IgD

IgE

IgG

IgM

• Monoclonal gammopathies
• Multiple myeloma (increased IgA, IgD, IgE, IgG)
• Waldenstrom's Macroglobulinemia (increased IgM)

Is caused by inherited immunodeficiency disorders (faulty plasma cell function).

• Heme protein found in cardiac and striated skeletal muscle.
• Function is to reversibly bind oxygen.

• Seen in skeletal or cardiac muscle damage.
• Early indicator of acute myocardial infarction.

• Inhibitory protein found in cardiac muscle.
• Functions to bind calcium, permitting contraction of the heart muscle.

• Seen in acute myocardial infarction (AMI).
• Remain elevated for about 1 week after AMI.

• C-reactive protein (CRP): can increase up to 1000%
• Alpha-1 antitrypsin: increases by 200-400%
• Fibrinogen: increases by 200-400%
• Haptoglobin: increases by 200-400%
• Complement proteins: increase by 50%
• Ceruloplasmin