1

Commonly used lab values at a glance

Chem 7
Normal Ranges (adult ranges) Panic Values
Na+ Sodium 136-145 mEq/L <120 or >160 mEq/L
K+ Potasium 3.5 - 5.0 mEq/L <2.5 or >6.5 mEq/L
Cl- Chloride 98 - 106 mEq/L <80 or >115 mEq/L
sCO2 Carbonic acid-bicarbonate buffer system 23 - 30 mEq/L <6 mEq/L
Gluc(f) Glucose (fasting) 70-105 mg/dL <40(♀);50(♂) & >400 mg/dL
BUN Blood Urea Nitrogen 10-20 mg/dL >100 mg/dL
Cr Creatinine 0.5-1.1(♀); 0.6-1.2 (♂) mg/dL >4.0 mg/dL

Chem 10
Chem 7 All of the above tests
Ca2+ Ionized calcium 4.5 - 5.6 mg/dL <2.2 or >7.0 mg/dL
Ca Free calcium 9.0 - 10.5 mg/dL <6.0 or >13 mg/dL
Mg2+ Magnesium 1.3 - 2.1 mEq/L <0.5 or > 3.0 mEq/L
PO4- Phosphate 3.0 - 4.5 mg/dL <1.0 mg/dL

Chem Physio Hyper Hypo Comments

Dehydration (excessive sweating, CHF, cirrhosis, vomiting, diarrhea, Spurious hyponatremia may be
Na+ Na+ is the predominant
extracellular cation. The serum severe vomiting, or diarrhea), exercise, excessive sweating (with produced by severe lipemia or
Na+ level is primarily determined polyuria (diabetes mellitus, replacement of water but not salt, hyperproteinemia if Na+ analysis
diabetes insipidus), eg, marathon running), salt-losing involves a dilution step.
by the volume status of the
hyperaldosteronism, inadequate nephropathy, adrenal insufficiency, The serum Na+ falls about 1.6
individual. Hyponatremia can be water intake (coma, hypothalamic nephrotic syndrome, water meq/L for each 100 mg/dL
divided into hypovolemia, disease). intoxication, SIADH, AIDS. increase in blood glucose.
euvolemia, and hypervolemia Hyponatremia in a normovolemic
categories. Drugs: steroids, licorice, oral Drugs: thiazides, diuretics, ACE patient with urine osmolality
contraceptives. inhibitors, chlorpropamide, higher than plasma osmolality
carbamazepine, antidepressants suggests the possibility of SIADH,
(SSRIs), antipsychotics. myxedema, hypopituitarism, or
reset osmostat.
Treatment of disorders of Na+
balance relies on clinical
assessment of the patient's
extracellular fluid volume rather
than the serum Na+.
Massive hemolysis, severe tissue Low K+ intake, prolonged vomiting
K+ K+ is predominantly an
intracellular cation whose plasma damage, rhabdomyolysis, or diarrhea, renal tubular acidosis
Spurious hyperkalemia can occur
with hemolysis of sample, delayed
level is regulated by renal acidosis, dehydration, acute or types I and II, separation of serum from
chronic renal failure, Addison hyperaldosteronism, Cushing
excretion. erythrocytes, prolonged fist
disease, renal tubular acidosis syndrome, osmotic diuresis (eg,
type IV (hyporeninemic hyperglycemia), alkalosis, familial clenching during blood drawing,
Plasma K+concentration
hypoaldosteronism), periodic paralysis, trauma and prolonged tourniquet
determines neuromuscular
hyperkalemic familial periodic (transient), subarachnoid placement. Very high white blood
irritability. Elevated or depressed
paralysis, exercise (transient). hemorrhage, genetic hypokalemic cell or platelet counts may cause
K+concentrations interfere with salt-losing tubulopathies such as spurious elevation of serum K+,
muscle contraction. Drugs: K+salts, K+-sparing Gitelman syndrome (familial but plasma K+ levels are normal.
diuretics (eg, spironolactone, hypokalemia-hypocalciuria-
triamterene, eplerenone), hypomagnesemia).
nonsteroidal anti-inflammatory
drugs, β-blockers, ACE inhibitors, Drugs: adrenergic agents
ACE-receptor blockers, high-dose (isoproterenol), diuretics.
trimethoprim- sulfamethoxazole.
Cl-, the principal inorganic anion Renal failure, nephrotic Vomiting, diarrhea, gastrointestinal Test is helpful in assessing normal
Cl- of extracellular fluid, is important syndrome, renal tubular acidosis, suction, renal failure combined and increased anion gap
in maintaining normal acid–base dehydration, overtreatment with with salt deprivation, over- metabolic acidosis. It is somewhat
balance and normal osmolality. saline, hyperparathyroidism, treatment with diuretics, chronic helpful in distinguishing
If Cl- is lost (as HCl or NH4Cl), diabetes insipidus, metabolic respiratory acidosis, diabetic hypercalcemia due to primary
alkalosis ensues; if Cl- is acidosis from diarrhea (loss of ketoacidosis, excessive sweating, hyperparathyroidism (high serum
ingested or retained, acidosis HCO3–), respiratory alkalosis, SIADH, salt-losing nephropathy, Cl-) from that due to malignancy
ensues. hyperadrenocorticism. acute intermittent porphyria, water (normal serum Cl-).
intoxication, expansion of
Drugs: acetazolamide extracellular fluid volume, adrenal
(hyperchloremic acidosis), insufficiency, hyperaldosteronism,
androgens, hydrochlorothiazide, metabolic alkalosis.
salicylates (intoxication).
Drugs: chronic laxative or
bicarbonate ingestion,
corticosteroids, diuretics.
 2

Chem Physio Hyper Hypo Comments

sCO2/ Bicarbonate-carbonic acid buffer is
one of the most important buffer
Primary metabolic alkalosis,
compensated respiratory acidosis,
Metabolic acidosis, compensated
respiratory alkalosis. Fanconi
Total CO2 determination is
indicated for all seriously ill
-
HCO3 systems in maintaining normal
body fluid pH.
volume contraction,
mineralocorticoid excess,
syndrome, volume overload. patients on admission.
If arterial blood gas studies are
congenital chloridorrhea. Drugs: acetazolamide, outdated done, total CO2 test is redundant.
Total CO2 is measured as the sum tetracycline.
of bicarbonate concentration plus Drugs: diuretics (eg, thiazide, Simultaneous measurement of
carbonic acid concentration plus furosemide). pH and PCO2 is required to fully
dissolved CO2. characterize a patient's acid–
base status.
Because bicarbonate makes up
90–95% of the total CO2 content,
total CO2 is a useful surrogate for
bicarbonate concentration.
Normally, the glucose Diabetes mellitus, Cushing Pancreatic islet cell disease with Diagnosis of diabetes mellitus
Gluc concentration in extracellular fluid syndrome (10–15%), chronic increased insulin, insulinoma, requires a fasting plasma glucose
is closely regulated so that a pancreatitis (30%). adrenocortical insufficiency, of >126 mg/dL on more than one
source of energy is readily hypopituitarism, diffuse liver occasion or a casual plasma
available to tissues and so that no Drugs: corticosteroids, phenytoin, disease, malignancy glucose level ≥200 mg/dL
glucose is excreted in the urine. estrogen, thiazides. (adrenocortical, stomach, (11.1mmol/L) along with
fibrosarcoma), infant of a symptoms of diabetes.
diabetic mother, enzyme
deficiency diseases (eg, Hypoglycemia is defined as a
galactosemia). glucose of <50 mg/dL in men
and <40 mg/dL in women.
Drugs: insulin, ethanol,
propranolol; sulfonylureas, While random serum glucose
tolbutamide, and other oral levels correlate with home
hypoglycemic agents. glucose monitoring results
(weekly mean capillary glucose
values), there is wide fluctuation
within individuals. Thus,
glycosylated hemoglobin levels
are favored to monitor glycemic
control.
Urea, an end product of protein Renal failure (acute or chronic), Hepatic failure, nephrotic
BUN metabolism, is excreted by the urinary tract obstruction, syndrome, cachexia (low-protein
Urease assay method commonly
used.
kidney. dehydration, shock, burns, CHF, and high-carbohydrate diets).
GI bleeding. Nephrotoxic drugs BUN/Cr ratio (normally 12:1–
BUN is directly related to protein (eg, gentamicin). 20:1) is decreased in acute
intake and nitrogen metabolism tubular necrosis, advanced liver
and inversely related to the rate of disease, low protein intake, and
excretion of urea.
following hemodialysis.
Urea concentration in glomerular BUN/Cr ratio is increased in
filtrate is the same as in plasma, dehydration, GI bleeding, and
but its tubular reabsorption is
increased catabolism.
inversely related to the rate of
urine formation.

Thus, the BUN is a less useful

measure of glomerular filtration
rate than the serum creatinine
(Cr).
Acute or chronic renal failure, Reduced muscle mass. Patients with diabetic
Cr Endogenous creatinine is excreted
by filtration through the urinary tract obstruction, ketoacidosis may have spuriously
glomerulus and by tubular nephrotoxic drugs, elevated Cr.
hypothyroidism.
secretion. Creatinine clearance is
Cephalosporins may spuriously
an acceptable clinical measure of increase or decrease Cr
glomerular filtration rate (GFR), measurement.
although it sometimes Increased bilirubin may
overestimates GFR (eg, in spuriously decrease Cr.
cirrhosis).
Chronic renal insufficiency may
For each 50% reduction in GFR, be underrecognized. Age, male
serum creatinine approximately gender, and black race are
doubles. predictors of kidney disease.

Serum creatinine levels

frequently do not reflect
decreased renal function because
creatinine production rate is
decreased with reduced lean
body mass. Increased
intravascular volume and
increased volume of distribution
associated with anasarca may
also mask decreased renal
function by reducing serum
creatinine levels.
 3

Chem Physio Hyper Hypo Comments

High cardiac output, exercise, Acute or chronic renal failure,
CrCl Widely used test of glomerular
filtration rate. Theoretically acromegaly, diabetes mellitus decreased renal blood flow
Serum Cr may, in practice, be a
more reliable indicator of renal
reliable, but often compromised by (early stage), infections, (shock, hemorrhage, function than 24-hour ClCr unless
hypothyroidism. dehydration, CHF).
incomplete urine collection. urine collection is carefully
Drugs: nephrotoxic drugs. monitored. An 8-hour collection
Creatinine clearance is calculated
provides results similar to those
from measurement of urine
obtained with a 24-hour
creatinine (UCr [mg/dL]),
collection.
plasma/serum creatinine (PCr
[mg/dL]), and urine flow rate (V ClCr will overestimate glomerular
[mL/min]) according to the filtration rate to the extent that
formula: Cr is secreted by the renal
tubules (eg, in cirrhosis).

ClCr can be estimated from the

serum creatinine using the
where following formula:

Serial decline in ClCr is the most

Creatinine clearance is often reliable indicator of progressive
"corrected" for body surface area renal dysfunction.
(BSA [m2]) according to the
formula:

Serum calcium is the sum of Hyperparathyroidism, Hypoparathyroidism, vitamin D Need to know serum albumin to
Ca ionized calcium plus complexed malignancies secreting parathyroid deficiency, renal insufficiency, interpret calcium level. For every
calcium and calcium bound to hormone–related protein (PTHrP) pseudohypoparathyroidism, decrease in albumin by 1 mg/dL,
proteins (mostly albumin). (especially squamous cell magnesium deficiency, calcium should be corrected
Level of ionized calcium is carcinoma of lung and renal cell hyperphosphatemia, massive upward by 0.8 mg/dL. In 10% of
regulated by parathyroid hormone carcinoma), vitamin D excess, transfusion, hypoalbuminemia. patients with malignancies,
and vitamin D. milk-alkali syndrome, multiple hypercalcemia is attributable to
myeloma, Paget disease of bone coexistent hyperparathyroidism,
with immobilization, sarcoidosis, suggesting that serum PTH levels
other granulomatous disorders, should be measured at initial
familial hypocalciuria, vitamin presentation of all hypercalcemic
Aintoxication, thyrotoxicosis, patients
Addison disease. Drugs: antacids
(some), calcium salts, chronic
diuretic use (eg, thiazides),
lithium, others.
Calcium circulates in three forms: Reduced blood pH (more acidic). Elevated blood pH (more Ionized calcium measurements
Ca2+ 1) free Ca2+ (47%) alkaline). are not needed except in special
2) protein-bound to albumin and circumstances, eg, massive
globulins (43%) blood transfusion, liver
3) calcium-ligand complexes transplantation, neonatal
(10%) (with citrate, bicarbonate, hypocalcemia, cardiac surgery,
lactate, phosphate, and sulfate). and possibly monitoring of
patients with secondary
Protein binding is highly pH- hyperparathyroidism from renal
dependent, and acidosis results in failure.
an increased free Ca2+fraction.
Ionized Ca2+ is the form that is
physiologically active.

Ionized calcium is a more accurate

reflection of physiologic status
than total calcium in patients with
altered serum proteins (renal
failure, nephrotic syndrome,
multiple myeloma, etc), altered
concentrations of calcium-binding
ligands, and acid–base
disturbances.
 4

Chem Physio Hyper Hypo Comments

Magnesium is primarily an Dehydration, tissue trauma, renal Chronic diarrhea, enteric fistula, Magnesium deficiency correlates
Mg2+ intracellular cation (second most failure, hypoadrenocorticism, starvation, chronic alcoholism, total with higher mortality and poorer
abundant, 60% found in bone); it hypothyroidism. parenteral nutrition with inadequate clinical outcome in the ICU and is
is a necessary cofactor in replacement, hypoparathyroidism directly implicated in
numerous enzyme systems, Drugs: aspirin (prolonged use), (especially post parathyroid hypokalemia, hypocalcemia,
particularly ATPases. lithium, magnesium salts, surgery), acute pancreatitis, chronic tetany, and dysrhythmia.
progesterone, triamterene. glomerulonephritis,
By regulating enzymes controlling hyperaldosteronism, diabetic Hypomagnesemia is associated
intracellular calcium, Mg2+ affects ketoacidosis, CHF, critical illness, with tetany, weakness,
smooth muscle vasoconstriction, Gitelman syndrome (familial disorientation, and somnolence.
important to the underlying hypokalemia–hypomagnesemia–
pathophysiology of several critical hypocalciuria), hereditary isolated A magnesium deficit may exist
illnesses. magnesium wasting, induced with little or no apparent change
hypothermia. in serum level.
In extracellular fluid, it influences
neuromuscular response and Drugs: albuterol, amphotericin B, There is a progressive reduction
irritability. calcium salts, cisplatin, citrates in serum magnesium level during
(blood transfusion), cyclosporine, normal pregnancy (related to
Magnesium concentration is diuretics, ethacrynic acid hemodilution).
determined by intestinal
absorption, renal excretion, and
exchange with bone and
intracellular fluid.
The plasma concentration of Renal failure, calcific uremic Hyperparathyroidism, Maintenance of a normal serum
PO4- inorganic phosphate is determined arteriolopathy (calciphylaxis), hypovitaminosis D (rickets, phosphorus level depends chiefly
by parathyroid gland function, tumor lysis syndrome, massive osteomalacia), malabsorption upon regulation of phosphorus
action of vitamin D, intestinal blood transfusion, (steatorrhea), malnutrition, reabsorption by the kidney. The
absorption, renal function, bone hypoparathyroidism, sarcoidosis, starvation or cachexia, refeeding majority of this reabsorption
metabolism, and nutrition. neoplasms, adrenal insufficiency, syndrome, bone marrow (80%) occurs in the proximal
acromegaly, hypervitaminosis D, transplantation, renal phosphate tubule and is mediated by the
Serum phosphorus concentrations osteolytic metastases to bone, wasting due to autosomal dominant sodium-phosphate cotransporter
have a circadian rhythm (highest leukemia, milk-alkali syndrome, or X-linked dominant (NaPi-II). Parathyroid hormone,
level in late morning, lowest in healing bone fractures, hypophosphatemic rickets, GH via a variety of intracellular
evening) and are subject to rapid pseudohypoparathyroidism, deficiency, chronic alcoholism, signaling cascades leading to
change secondary to diabetes mellitus with ketosis, severe diarrhea, vomiting, NaPi-IIa internalization and
environmental factors such as diet malignant hyperpyrexia, cirrhosis, nasogastric suction, acute downregulation, is the main
(carbohydrate), phosphate-binding lactic acidosis, respiratory pancreatitis, severe hypercalcemia regulator of renal phosphate
antacids, and fluctuations in GH, acidosis. (any cause), acute gout, osteoblastic reabsorption. In renal
insulin, and renal function. There metastases to bone, severe burns insufficiency, phosphorus
is also a seasonal variation with Drugs: phosphate infusions or (diuretic phase), respiratory excretion declines and
maximum levels in May and June enemas, anabolic steroids, alkalosis, hyperalimentation with hyperphosphatemia develops.
(low levels in winter). ergocalciferol, furosemide, inadequate phosphate repletion, The body's homeostatic
hydrochlorothiazide, clonidine, carbohydrate administration (eg, mechanisms cause secondary
During first decade of menopause, verapamil, potassium intravenous D50W glucose bolus), hyperparathyroidism and renal
values increase ~0.2 mg/dL supplements, and others. renal tubular acidosis and other osteodystrophy.
(~0.06 mmol/L). Bedrest causes renal tubular defects, diabetic
increase up to 0.5 mg/dL (0.16 Thrombocytosis may cause ketoacidosis (during recovery), acid– Shift of phosphorus from
mmol/L). Ingestion of food may spurious elevation of serum base disturbances, hypokalemia, extracellular to intracellular
cause a transient decrease in phosphate, but plasma phosphate pregnancy, hypothyroidism, compartments, decreased
blood levels. Low values are also levels are normal. hemodialysis. gastrointestinal absorption, and
seen during menstruation. increased urinary losses, are the
Drugs: acetazolamide, phosphate- primary mechanisms of
binding antacids, anticonvulsants, β- hypophosphatemia.
adrenergic agonists, catecholamines,
estrogens, isoniazid, oral Hypophosphatemia has been
contraceptives, prolonged use of implicated as a cause of
thiazides, glucose infusion, insulin rhabdomyolysis, respiratory
therapy, salicylates (toxicity). failure, hemolysis, and left
ventricular dysfunction.
 5
Inflammatory Lab Tests
C-reactive Protein C-RP or CRP (normal findings <1.0 mg/dL)
Physio Interpretation Comments
CRP is an acute-phase reactant protein. Hepatic Increased in: inflammatory states, including CRP is a very sensitive but nonspecific marker of
secretion is stimulated in response to arteriosclerotic disorders. inflammation. A variety of conditions other than
inflammatory cytokines. Unlike other acute arteriosclerosis may cause dramatic increases in
phase proteins, CRP is not affected by hormones. CRP levels. CRP levels increase within 2 hours of
CRP activates the complement system, binds to acute insult (eg, surgery, infection) and should
Fc receptors, and serves as an opsonin for some peak and begin decreasing within 48 hours if no
microorganisms. other inflammatory event occurs. In patients
with rheumatoid arthritis, persistently elevated
Rapid, marked increases in CRP occur with CRP concentrations are present when the disease
inflammation, infection, trauma and tissue is active and usually fall to normal during periods
necrosis, malignancies, and autoimmune of complete remission.
disorders.
Patients with high hs-CRP concentrations are
CRP levels are not only valuable in the clinical more likely to develop stroke, myocardial
assessment of chronic inflammatory disorders, infarction, and severe peripheral vascular
but also in assessing vascular inflammation and disease. hs-CRP results are used to assign risk as
cardiovascular risk stratification. CRP level has follows: <1.0 mg/L lowest tertile, lowest risk;
been shown to be an independent risk factor for 1.0–3.0 mg/L middle tertile, average risk; >3.0
atherosclerotic disease. Elevated CRP levels are mg/L highest tertile, highest risk.
associated with increased cardiovascular
morbidity and mortality in patients with coronary Noncardiovascular cause should be considered if
artery disease. CRP values are >10 mg/dL with repeat
measurements.

Erythrocyte Sedimentation Rate Sed Rate or ESR (normal findings ≤20 [♀] ≤15[♂] mm/hr)
Physio Interpretation Comments
In plasma, erythrocytes (red blood cells [RBCs]) Increased in: Infections (osteomyelitis, pelvic There is a good correlation between ESR and C-
usually settle slowly. However, if they aggregate inflammatory disease [75%]), inflammatory reactive protein, but ESR is less expensive.
for any reason (usually because of plasma disease (temporal arteritis, polymyalgia
proteins called acute-phase reactants, eg, rheumatica, rheumatic fever), Test is useful and indicated only for diagnosis
fibrinogen), they settle rapidly. malignantneoplasms, paraproteinemias, anemia, and monitoring of temporal arteritis, and
pregnancy, chronic renal failure, GI disease polymyalgia rheumatica. The test is not sensitive
Sedimentation of RBCs occurs because their (ulcerative colitis, regional ileitis). For or specific for other conditions.
density is greater than plasma. endocarditis, sensitivity is approximately 93%.
ESR is higher in women, blacks, and older
ESR measures the distance in millimeters that Decreased in: Polycythemia, sickle cell anemia, persons.
erythrocytes fall during 1 hour. spherocytosis, anisocytosis, poikilocytosis,
hypofibrinogenemia, hypogammaglobulinemia,
congestive heart failure, microcytosis, certain
drugs (eg, high-dose corticosteroids).

Cardiac Markers
HOURS DAYS
Enzyme Begins to Peaks Returns to Normal
Rise
Total CPK 4-6 24 3-4
CK-MB 4 18 2
AST 8 24-48 4
LDH 24 72 8-9
Troponin T 4-6 10-24 10
Troponin I 4-6 10-24 4
Copied from: Pagana, KD and Pagana, TJ. Mosby’s Manual of Diagnostic and Laboratory Tests: Second Edition. pg 192 (2002)
 6
Troponin I cardiac Troponin I (cTnI) (normal findings <0.03 ng/mL)
Troponin T2 cardiac Troponin T2 (cTnT2) (normal findings <0.20 ng/mL)
Used to diagnose AMI; increases rapidly 3–12 h after MI, peak at 24 h, and may stay
elevated for several days (Troponin I 5–7 d, Troponin T up to 14 d). Serial testing
recommended. More cardiac-specific than CK-MB
Test positive with myocardial damage, including MI, & myocarditis; renal failure can
cause a false-positive result. Also they are falsely elevated in dialysis patients.

CK-MB Creatine Phosphokinase II -- produced primarily by the heart (normal value ≤ 6% of total CPK)
Used in suspected MI or muscle diseases. Heart, skeletal muscle, and brain have high
levels.
Increased with muscle damage (AMI, myocarditis, muscular dystrophy, muscle trauma
[including injections], aftermath of surgery), brain infarction, defibrillation, cardiac
catheterization and surgery, rhabdomyolysis, polymyositis, hypothyroidism
CPK Isoenzymes
MB: (normal < 6%, heart origin) increased in ami (begins in 2–12 h, peaks at 12–40 h,
returns to normal in 24–72 h); troponin is marker of choice for ami; pericarditis with
myocarditis, rhabdomyolysis, crush injury, duchenne muscular dystrophy, polymyositis,
malignant hyperthermia, cardiac surgery
MM: (normal 94–100%, skeletal muscle origin) increased in crush injury, malignant
hyperthermia, seizures, im injections
BB: (normal 0%, brain origin) brain injury (cva, trauma), metastatic neoplasms (eg,
prostate), malignant hyperthermia, colonic infarction

Myoglobin The ferrous globin complex responsible for the red color in muscles (normal value <90 μg/L)
Increases 6–12 h after AMI. Skeletal muscle injury (crush, injection, surgical
procedure), delirium tremens, rhabdomyolysis (burns, seizures, sepsis, hypokalemia,
others),

BNP B-Natriuretic Peptide (normal value 0-100 pg/mL)

It is released by the ventricular myocardium secondary to volume and pressure
overload. BNP increases sodium and water excretion. CHF severity correlates with
BNP level (< 100 pg/mL rules out CHF, 100–400 pg/mL is borderline, > 400 pg/mL is
highly suggestive of CHF). BNP used to differentiate CHF and other causes of
dyspnea (eg, COPD). Increased in CHF & left ventricular dysfunction. The test is not
suitable for being the sole criterion because its sensitivity is 90%, & its specificity is
73%.

Lipid Panel
Total Cholesterol (tCh) (Desirable < 200 mg/dL; Borderline 200-239 mg/dL; High risk >240 mg/dL)
Physio Interpretation Comments
Cholesterol level is determined by lipid Increased in: Primary disorders: polygenic
metabolism, which is in turn influenced by hypercholesterolemia, familial
heredity, diet, and liver, kidney, thyroid, and hypercholesterolemia (deficiency of LDL
other endocrine organ functions. Screening for receptors), familial combined hyperlipidemia,
total cholesterol (TC) may be done with familial dysbetalipoproteinemia. Secondary
nonfasting specimens, but a complete lipoprotein disorders: hypothyroidism, uncontrolled diabetes
profile or LDL cholesterol (LDL-C) determination mellitus, nephrotic syndrome, biliary obstruction,
must be performed on fasting specimens. anorexia nervosa, hepatocellular carcinoma,
Cushing syndrome, acute intermittent porphyria.
Triglyceride (TG), and high-density lipoprotein Drugs: corticosteroids.
cholesterol (HDL-C) are directly measured.
Although methods have been developed for Decreased in: Severe liver disease (acute
direct LDL-C measurement, in practice, LDL-C is hepatitis, cirrhosis, malignancy),
often indirectly determined by use of the hyperthyroidism, severe acute or chronic illness,
Friedewald equation: malnutrition, malabsorption (eg, HIV), extensive
[LDL-C] = [TC] – [HDL-C] – [TG] / 5. burns, familial (Gaucher disease, Tangier
disease), abetalipoproteinemia, intestinal
Note: calculation is not valid for specimens lymphangiectasia.
having TG >400 mg/dL [>4.52 mmol/L], for
patients with type III hyperlipoproteinemia or
chylomicronemia, or nonfasting specimens.
 7
Triglycerides (Normal range: < 165 mg/dL)
Physio Interpretation Comments
Dietary fat is hydrolyzed in the small intestine, Increased in: Hypothyroidism, diabetes If serum is clear, the serum triglyceride level is
absorbed and resynthesized by mucosal cells, mellitus, nephrotic syndrome, chronic generally <350 mg/dL.
and secreted into lacteals as chylomicrons. alcoholism (fatty liver), biliary tract
obstruction, stress, familial lipoprotein lipase Elevated triglycerides are now considered an
Triglycerides in the chylomicrons are cleared deficiency, familial dysbetalipoproteinemia, independent risk factor for coronary artery
from the blood by tissue lipoprotein lipase. familial combined hyperlipidemia, obesity, the disease, and a major risk factor for acute
metabolic syndrome, viral hepatitis, cirrhosis, pancreatitis, particularly when serum
Endogenous triglyceride production occurs in pancreatitis, chronic renal failure, gout, triglyceride levels are >1000 mg/dL.
the liver. These triglycerides are transported in pregnancy, glycogen storage diseases types I,
association with β-lipoproteins in very low III, and VI, anorexia nervosa, dietary excess.
density lipoproteins.
Drugs: β-blockers, cholestyramine,
corticosteroids, diazepam, diuretics, estrogens,
oral contraceptives.

Decreased in: Tangier disease (α-lipoprotein

deficiency), hypo- and abetalipoproteinemia,
malnutrition, malabsorption, parenchymal liver
disease, hyperthyroidism, intestinal
lymphangiectasia.

Drugs: ascorbic acid, clofibrate, nicotinic acid,

gemfibrozil.

Lipoproteins
Because triglycerides and cholesterol are insoluble in water, they do not circulate freely in the blood. Instead they are transported to
and from tissues bound to different lipoproteins. Lipoproteins vary in their relative fat-protein composition, but they all contain
triglycerides, phospholipids, cholesterol, & protein.
HDL - High Density Lipoproteins
Physio- approximates Interpretation Comments
Density: 1.063 - 1.210 g/mL Increased in: Familial hyper-α-lipoproteinemia,
Diameter: 5 - 13 nm Pregnancy, wt reduction
Structural components: ~10%
Protein: ~50% Decreased in: Obesity, “metabolic syndrome
Lipid fractions: ~40% (insulin resistance, hyperglyceridemia),
Free Cholesterol: 3 - 4% malnutrition, sedentary lifestyle, cigarette
Esterified Cholesterol: 12% smoking, familial.
Phospholipid: 20 - 25%
Triglycerides: 3% Drugs: β-blockers (short-term effect)

LDL- Low Density Lipoproteins

Physio Interpretation Comments
Density: 1.019 - 1.063 g/mL Increased in: hyperlipoproteinemia, Nephrotic
Diameter: 20 - 28 nm Syndrome, Pregnancy, hemodialysis, biliary
Structural components: 10% obstruction, CAD, Diabetes, hypothyroidism,
Protein: ~20 - 25% anorexia nervosa
Lipid fractions: ~65 - 70%
Free Cholesterol: 7 - 10% Decreased in: Tangier dz, hyperthyroidism,
Esterified Cholesterol: 35 - 40% malnutrition, inflammatory joint dz, COPD, Wt
Phospholipid: 15 - 20% reduction, chronic anemia, Reye’s dz.
Triglycerides: 7 - 10%
 8
Liver Function Tests
ALT Alanine aminotransferase (Normal Range: 0 - 35 U/L)
Physio Interpretation Comments
Intracellular enzyme involved in amino acid Increased in: Acute viral hepatitis (ALT > ALT is the preferred enzyme for evaluation of
metabolism. AST), biliary tract obstruction (cholangitis, liver injury.
choledocholithiasis), alcoholic hepatitis and
Present in large concentrations in liver, kidney; cirrhosis (AST > ALT), liver abscess, metastatic ALT is more elevated than AST in viral
in smaller amounts, in skeletal muscle and or primary liver cancer; nonalcoholic hepatitis; AST elevated more than ALT in
heart. Released with tissue damage, steatohepatitis; right heart failure, ischemia or alcoholic hepatitis
particularly liver injury. hypoxia, injury to liver ("shock liver"),
extensive trauma. Drugs that cause cholestasis
or hepatotoxicity.

Decreased in: Pyridoxine (vitamin B6)

deficiency.

AST Aspartate aminotransferase (Normal Range: 0 - 35 U/L)

Physio Interpretation Comments
Intracellular enzyme involved in amino acid Increased in: Acute viral hepatitis (ALT > Test is NOT indicated for diagnosis of myocardial
metabolism. AST), biliary tract obstruction (cholangitis, infarction.
choledocholithiasis), alcoholic hepatitis and
Present in large concentrations in liver, cirrhosis (AST > ALT), liver abscess, metastatic AST/ALT ratio >1 suggests cirrhosis in patients
skeletal muscle, brain, red cells, and heart. or primary liver cancer; right heart failure, with hepatitis C.
Released into the bloodstream when tissue is ischemia or hypoxia, injury to liver ("shock
damaged, especially in liver injury. liver"), extensive trauma. ALT is more elevated than AST in viral
hepatitis; AST elevated more than ALT in
Decreased in: Pyridoxine (vitamin B6) alcoholic hepatitis.
deficiency [beriberi].

Alk Phos Alkaline Phosphatase (Normal Range: 41 - 133 IU/L)

Physio Interpretation Comments
Alkaline phosphatases are found in liver, bone, Increased in: Obstructive hepatobiliary disease, Alkaline phosphatase performs well in
intestine, and placenta. bone disease (physiologic bone growth, Paget measuring the extent of bone metastases in
disease, osteomalacia, osteogenic sarcoma, bone prostate cancer.
metastases), hyperparathyroidism, rickets,
benign familial hyperphosphatasemia, pregnancy Normal in osteoporosis.
(third trimester), GI disease (perforated ulcer or
bowel infarct), hepatotoxic drugs.

Decreased in: malnutrition, excess vitamin D

ingestion, pernicious anemia, Wilson disease,
hypothyroidism, zinc deficiency

GGT γ-glutamyl transferase (Normal Range: 9 - 85 U/L)

Parallels changes in serum alkaline phosphatase and 5'-nucleotidase in liver disease. Sensitive
indicator of alcoholic liver disease.
Physio Interpretation Comments
GGT is an enzyme present in liver, kidney, and Increased in: Liver disease: acute viral or toxic GGT is useful in follow-up of alcoholics
pancreas. hepatitis, chronic or subacute hepatitis, alcoholic undergoing treatment because the test is
hepatitis, cirrhosis, biliary tract obstruction sensitive to modest alcohol intake.
It is induced by alcohol intake and is an (intrahepatic or extrahepatic), primary or
extremely sensitive indicator of liver disease, metastatic liver neoplasm, and mononucleosis. GGT is elevated in 90% of patients with liver
particularly alcoholic liver disease. disease.
Drugs (by enzyme induction): phenytoin,
carbamazepine, barbiturates, alcohol. GGT is used to confirm hepatic origin of
elevated serum alkaline phosphatase.

Bilirubins
t-Bili total bilirubin
d-Bili direct or conjugated bilirubin
i-Bili indirect or unconjugated bilirubin
Physio Interpretation Comments
Bilirubin, a product of hemoglobin metabolism, is Increased in: Acute or chronic hepatitis, Assay of total bilirubin includes conjugated
conjugated in the liver to mono- and cirrhosis, biliary tract obstruction, toxic hepatitis, (direct) and unconjugated (indirect)
diglucuronides and excreted in bile. neonatal jaundice, congenital liver enzyme bilirubin plus delta bilirubin (conjugated
abnormalities (Dubin-Johnson, Rotor, Gilbert, bilirubin bound to albumin).
Some conjugated bilirubin is bound to serum Crigler-Najjar syndromes), fasting, hemolytic
albumin, so-called D (delta) bilirubin. disorders, and hemolysis. It is usually clinically unnecessary to
fractionate total bilirubin. The fractionation
is unreliable by the diazo reaction and may
underestimate unconjugated bilirubin. Only
conjugated bilirubin appears in the urine,
and it is indicative of liver disease;
hemolysis is associated with increased
unconjugated bilirubin.

Persistence of delta bilirubin in serum in

resolving liver disease means that total
bilirubin does not effectively indicate the
time course of resolution.
 9
Renal Fxn Tests
BUN Blood Urea Nitrogen
BUN:Cr Ratio Blood Urea Nitrogen to Creatinine = can also indicate GFR and therefore renal fxn.
Cr clearance (urine creatinine x Urine vol [24°])/serum creatinine = Creatinine clearance rate