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Pharmacy Student Survival Guide, 2e

Chapter 11. Interpretation of Clinical Laboratory Data

Electrolytes and Blood Chemistry

Electrolytes and blood chemistries are usually the first set of laboratory tests ordered upon initial patient presentation. Depending on the institution,
these tests may be ordered using different acronyms. A basic metabolic panel (BMP) includes sodium, potassium, chloride, carbon dioxide (CO2),

glucose, blood urea nitrogen (BUN), and creatinine.2 An abbreviated method for reporting the BMP is:

A comprehensive metabolic panel (CMP) includes albumin, alkaline phosphatase, alanine aminotransferase (ALT), aspartate aminotransferase (AST),
total bilirubin, and calcium, in addition to the components of the BMP. Other examples of biochemical profiles are SMA­6, SMA­12, and Chem Profile­
20.1

Sodium
Normal Range

135–147 mEq/L SI 135–147 mmol/L

Description

Sodium (Na+) is the most prevalent cation in the extracellular fluid.2 Sodium is important in regulating serum osmolality, fluid balance, and acid­base
balance. In addition, sodium also assists in maintaining the electric potential necessary for transmission of nerve impulses.2

Clinical Significance

Increased Sodium

Increased sodium (hypernatremia) may result from increased sodium intake or increased fluid loss.2,10 Thirst is the primary mechanism to prevent
hypernatremia, and, therefore, hypernatremia usually occurs in individuals who are unable to obtain adequate fluid intake. Fluid loss from
gastroenteritis, diabetes insipidus, Cushing disease, hyperaldosteronism, and administration of hypertonic saline solution are causes of
hypernatremia.10

Decreased Sodium

Decreased sodium (hyponatremia) may be caused by a decrease in total body sodium but is more commonly attributed to excess accumulation of body
water (dilutional hyponatremia).10

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depletion
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SIADH may be associated with disease states such as cancer or the use of medications, including chlorpropamide, thiazide diuretics, and
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Decreased sodium (hyponatremia) may be caused by a decrease in total body sodium but is more commonly attributed to excess accumulation of body
water (dilutional hyponatremia).10

Common causes of dilutional hyponatremia include CHF, cirrhosis, severe burns, chronic renal failure, and nephrotic syndrome.2,10 Sodium
depletion may also be seen in SIADH, cystic fibrosis, mineralocorticoid deficiency, or fluid replacement with solutions that do not contain sodium.10

SIADH may be associated with disease states such as cancer or the use of medications, including chlorpropamide, thiazide diuretics, and
carbamazepine.2

Potassium
Normal Range

3.5–5.2 meq/L SI 3.5–5.2 mmol/L

Description

Potassium (K+) is the main intracellular cation.2 Serum concentrations of potassium are not always an accurate indicator of potassium levels because
potassium is an intracellular ion. Potassium plays a key role in many bodily functions, including regulation of nerve excitability, acid­base balance, and
muscle function.2,10 Cardiac function and neuromuscular function can be significantly affected by either an increase or decrease in potassium levels.2

Clinical Significance

Increased Potassium

Causes of increased potassium (hyperkalemia) include metabolic or respiratory acidosis, renal failure, Addison disease, dehydration, and massive cell
damage from burns, injuries, and surgery.2,10 Medications such as angiotensin enzyme converting (ACE) inhibitors, angiotensin receptor blockers
(ARBs), potassium supplements, potassium­sparing diuretics, and oral contraceptives containing drospirenone are also contributing factors to
hyperkalemia.1,10

It is important to remember that a high potassium value may be reported if the specimen was hemolyzed when the laboratory test was performed.2,10

Decreased Potassium

Causes of decreased potassium (hypokalemia) include severe diarrhea and/or vomiting, respiratory alkalosis, hyperaldosteronism, Cushing disease,
alcoholism, and use of amphotericin B or thiazide, loop, or osmotic diuretics.1,2,10

If a patient is hypokalemic and potassium supplements have not helped to correct the low potassium, check to see if the magnesium is also low.
Decreased potassium is difficult to correct while magnesium remains low.10

Chloride
Normal Range

95–106 mEq/L SI 95–106 mmol/L

Description
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Chloride is the principal
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Serum chloride values are useful in identifying fluid or acid­base balance disorders.10
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95–106 mEq/L SI 95–106 mmol/L

Description

Chloride is the principal extracellular anion.2,10 Chloride primarily serves a passive role in the maintenance of fluid balance and acid­base balance.
Serum chloride values are useful in identifying fluid or acid­base balance disorders.10

Clinical Significance

Increased Chloride

Increased chloride (hyperchloremia) may be seen in metabolic acidosis, respiratory alkalosis, dehydration, diabetes insipidus, eclampsia, and renal
disorders.1,2,10

Decreased Chloride

Decreased chloride (hypochloremia) may be associated with prolonged vomiting, gastric suctioning, metabolic alkalosis, CHF, SIADH, Addison disease,
or use of acid suppressants (H2 blockers and proton pump inhibitors [PPIs]).10

Carbon Dioxide Content

Normal Range

22–30 mEq/L SI 22–30 mmol/L

Description

The majority of CO2 in the plasma is present as bicarbonate ions, and a small percentage is dissolved CO2. The CO2 content is the sum of both

bicarbonate ions and dissolved CO2.1 CO2 and bicarbonate are extremely important in regulating physiologic pH.1,11 It is important not to confuse the

terms CO2 content and CO2 gas (ie, pCO2). CO2 content is composed mostly of bicarbonate (HCO3−) and is a base. CO2 content is regulated by the

kidneys. CO2 gas is acidic and is regulated by the lungs.2

Clinical Significance

Increased CO2 Content

Increased CO2 is seen in metabolic alkalosis.1,2 Some common causes of metabolic alkalosis include diuretic therapy, primary aldosteronism, and

Bartter syndrome.2

Decreased CO2 Content

Decreased CO2 is associated with metabolic acidosis.1,2 Common causes of metabolic acidosis include diabetic ketoacidosis, methanol or salicylate

toxicity, lactic acidosis, and renal failure.2

Anion Gap
Normal Range
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3–11 mEq/L SI 3–11 mmol/L
toxicity, lactic acidosis, and renal failure.2
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Anion Gap
Normal Range

3–11 mEq/L SI 3–11 mmol/L

Description

The anion gap is calculated using the following formula:11

Anion gap is reflective of unmeasured acids.1 An increase in anion gap suggests an increase in the number of negatively charged weak acids in the
plasma.1,11 Anion gap is useful in evaluating causes of metabolic acidosis.11

Clinical Significance

Anion gap may be elevated in conditions such as renal failure, lactic acidosis, ketoacidosis, and salicylate, methanol, or ethylene glycol toxicity.1,11

Glucose
Normal Range

Fasting 70–110 mg/dL SI 3.9–6.1 mmol/L

Description

Glucose is an important energy source for most cellular functions.1 Blood glucose regulation is achieved through a complex set of mechanisms that
involves insulin, glucagon, cortisol, epinephrine, and other hormones.8

Clinical Significance

Increased Glucose

The most common cause of increased glucose (hyperglycemia) is diabetes mellitus.1,11,12 A fasting blood glucose greater than 126 mg/dL on two
occasions or a random blood glucose greater than 200 mg/dL (along with symptoms of diabetes) on two occasions is consistent with a diagnosis of
diabetes mellitus.12 Patients are diagnosed with impaired fasting glucose (IFG) if blood glucose levels are 100 to 125 mg/dL when fasting. Impaired
glucose tolerance (IGT) is defined as a random glucose level greater than or equal to 140 mg/dL but less than 200 mg/dL.12 Both IFG and IGT are
suggestive of prediabetes. Other causes of hyperglycemia include Cushing disease, sepsis, pancreatitis, shock, trauma, myocardial infarction, and use
of corticosteroids or niacin.13

Decreased Blood Glucose

Decreased blood glucose (hypoglycemia) may result from missing a meal, oral hypoglycemic agents, insulin overdose, or Addison disease.2,8,14

Blood Urea Nitrogen

Normal
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6–20 mg/dL SI 2.1–7.1 mmol/L

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Decreased blood glucose (hypoglycemia) may result from missing a meal, oral hypoglycemic agents, insulin overdose, or Addison disease.2,8,14

Blood Urea Nitrogen

Normal Range

6–20 mg/dL SI 2.1–7.1 mmol/L

Description

Urea nitrogen is an end product of protein catabolism.2 It is produced in the liver, transported in the blood, and cleared by the kidneys. BUN
concentration serves as a marker of renal function.7

Clinical Significance

Increased BUN

Increased BUN (azotemia) may be associated with acute or chronic renal failure, CHF, gastrointestinal bleeding (gut flora metabolizes blood to
ammonia and urea nitrogen), high­protein diet, shock, dehydration, antianabolic and nephrotoxic medications.2,7

Decreased BUN

Decreased BUN is seen in liver failure because of inability of the liver to synthesize urea, and in disease states such as SIADH and acromegaly.2,7

Creatinine
Normal Range

0.6–1.3 mg/dL SI 50–115 μmol/L

Description

Muscle creatine and phosphocreatine break down to form creatinine.2,7 Creatinine is released into the blood and excreted by glomerular filtration in
the kidneys.1 As long as muscle mass remains fairly constant, creatinine formation remains constant.7 An increase in serum creatinine in the face of
unchanged creatinine formation suggests a diminished ability of the kidneys to filter creatinine.7 Thus, serum creatinine is used as a tool to identify
patients with renal dysfunction.1,2

Clinical Significance

Increased Creatinine

Increased creatinine is associated with renal dysfunction, dehydration, urinary tract obstruction, vigorous exercise, hyperthyroidism, myasthenia
gravis, increased meat intake, and use of nephrotoxic drugs such as cisplatin and amphotericin B.2,7

Decreased Creatinine

Serum creatinine may be reduced in patients with cachexia, inactive elderly or comatose patients, and spinal cord injury patients.7

BUN/Creatinine
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Calculating the BUN/creatinine ratio may suggest an etiology for renal dysfunction. A BUN/creatinine ratio greater than 20 suggests a prerenal cause
such as GI bleeding. A BUN/creatinine ratio between 10 and 20 indicates intrinsic renal disease.2,7
gravis, increased meat intake, and use of nephrotoxic drugs such as cisplatin and amphotericin B.
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Decreased Creatinine

Serum creatinine may be reduced in patients with cachexia, inactive elderly or comatose patients, and spinal cord injury patients.7

BUN/Creatinine Ratio

Calculating the BUN/creatinine ratio may suggest an etiology for renal dysfunction.7 A BUN/creatinine ratio greater than 20 suggests a prerenal cause
such as GI bleeding. A BUN/creatinine ratio between 10 and 20 indicates intrinsic renal disease.2,7

Creatinine Clearance
This calculation provides an estimate of the glomerular filtration rate (GFR) and is a better indication of renal function than using serum creatinine
alone.7 In addition to assessing kidney function in patients with renal failure, the creatinine clearance (CrCl) can be used to monitor patients on
nephrotoxic medications and to assess need for renal dosing adjustments.7

The CrCl using the Cockroft and Gault formula is calculated as follows:7

The equation must be multiplied by 0.85 if the patient is female.

Calcium
Normal Range

8.5–10.8 mg/dL SI 2.1–2.7 mmol/L

Description

The majority of calcium (Ca2+) in the body (98%­99%) is found in the skeletal bones and teeth.2,10 The remainder is found in the blood, muscle, and
other tissues. In addition to playing a role in bone mineralization, calcium is important in cardiac and skeletal muscle contraction, blood coagulation,
enzyme activity, glandular activity, and transmission of nerve impulses.10 In the blood, approximately half of the calcium is in the ionized "free" state,
and the other half is bound to proteins or complexed with anions. Only calcium in the free state may be utilized in physiologic functions.10 Calcium
levels are regulated by a complex system that involves the skeleton, kidneys, intestines, parathyroid hormone, vitamin D, and serum phosphate.2,10

Clinical Significance

Increased Calcium

The most common causes of increased calcium (hypercalcemia) are malignancies and primary hyperparathyroidism.2,10 Other causes include Paget
disease, sarcoidosis, vitamin D intoxication, milk­alkali syndrome, Addison disease, and use of thiazide diuretics and lithium.

Decreased Calcium

Causes of decreased calcium (hypocalcemia) include hypoparathyroidism, vitamin D deficiency, hyperphosphatemia, acute pancreatitis, alkalosis,
alcoholism, renal disease, and use of loop diuretics.2,10

Pseudohypocalcemia

Approximately one­half of circulating serum calcium is bound to plasma proteins such as albumin.2,10 A decreased albumin concentration may lead to
a decreased total serum calcium concentration, and calcium levels may appear falsely low in the presence of low albumin.2 Serum calcium levels may
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Inorganic Phosphorus
alcoholism, renal disease, and use of loop diuretics.2,10
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Pseudohypocalcemia

Approximately one­half of circulating serum calcium is bound to plasma proteins such as albumin.2,10 A decreased albumin concentration may lead to
a decreased total serum calcium concentration, and calcium levels may appear falsely low in the presence of low albumin.2 Serum calcium levels may
be corrected for low albumin as follows:

Inorganic Phosphorus
Normal Range

2.5–5 mg/dL SI 0.8–1.6 mmol/L

Description

Phosphate (PO4) is an intracellular anion involved in several critical physiologic functions.10 Phosphate is necessary for formation of the cellular
energy source adenosine triphosphate (ATP) and the synthesis of phospholipids. Phosphate also plays a role in protein, fat, and carbohydrate
metabolism, as well as acid­base balance.2 Phosphate has an inverse relationship with calcium.10

Clinical Significance

Increased Phosphate

Increased phosphate (hyperphosphatemia) can result from renal dysfunction, increased vitamin D intake, increased phosphate intake,
hypoparathyroidism, bone malignancy, and use of laxatives.2

Decreased Phosphate

Decreased phosphate (hypophosphatemia) can be associated with overuse of aluminum­ and calcium­containing antacids (these bind phosphorus in
the GI tract), alcoholism, malnutrition, hyperparathyroidism, and respiratory alkalosis.2,10

Magnesium
Normal Range

1.5–2.6 mg/dL SI 0.75–1.2 mmol/L

Description

Magnesium (Mg2+) is a necessary cofactor in physiologic functions utilizing ATP.2 It is also vital in protein and nucleic acid synthesis, carbohydrate
metabolism, and contraction of muscle tissue.2

Clinical Significance

Increased Magnesium

Increased magnesium (hypermagnesemia) may result from renal failure or Addison disease.2 In addition, the administration of Mg supplements or Mg­
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Decreased Magnesium
metabolism, and contraction of muscle tissue.
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Clinical Significance

Increased Magnesium

Increased magnesium (hypermagnesemia) may result from renal failure or Addison disease.2 In addition, the administration of Mg supplements or Mg­
containing antacids or laxatives to patients with renal dysfunction may also result in hypermagnesemia.2,10

Decreased Magnesium

Reduced magnesium (hypomagnesemia) may be associated with diarrhea, renal wasting, vomiting, malabsorption, alcoholism, hyperaldosteronism,
chronic pancreatitis, diabetes mellitus, hypercalcemia, and use of loop diuretics, amphotericin B, or cisplatin.2,10

Uric Acid
Normal Range

Male 3.4–8.5 mg/dL SI 202–506 μmol/L

Females 2.3–6.6 mg/dL SI 137–393 μmol/L

Description

Uric acid is the main metabolic end product of the purine bases of DNA.2,15

Clinical Significance

Increased Uric Acid

Increased uric acid (hyperuricemia) may be caused by excessive production of purines or inability of the kidney to excrete urate.15 Common causes of
hyperuricemia are renal dysfunction, metabolic acidosis, tumor lysis syndrome, purine­rich diet, and use of furosemide, thiazide diuretics, and
niacin.2,15

Hyperuricemia may be associated with the development of gouty arthritis, nephrolithiasis, and gouty tophi.2

Decreased Uric Acid

Decreased uric acid levels (hypouricemia) are usually of little clinical significance but may occur with a low­protein diet, deficiency of xanthine oxidase,
or use of allopurinol, probenecid, or high doses of aspirin or vitamin C.2,15

Osmolality
Normal Range

280–303 mOsm/kg SI 280–303 mmol/kg

Description

Plasma osmolality describes the osmotic concentration or number of osmotically active particles in the plasma.2 It can be used to evaluate water and
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Description

Plasma osmolality describes the osmotic concentration or number of osmotically active particles in the plasma.2 It can be used to evaluate water and
electrolyte balance. Sodium, glucose, and BUN are the main components that determine serum osmolality.2 The serum osmolality may be calculated
as follows:

Clinical Significance

Increased Serum Osmolality

Increased serum osmolality (hyperosmolality) may occur with dehydration, diabetic ketoacidosis, and ethanol, methanol, or ethylene glycol toxicity.2

Decreased Serum Osmolality

Decreased serum osmolality may be caused by overhydration, hyponatremia, or diabetes insipidus.2

Total Serum Protein

Normal Range

6.0–8.5 g/dL SI 60–85 g/L

Description

The total serum protein is the sum of albumin, globulins, and other circulating proteins in the serum.2 Albumin and globulins are indicators of
nutritional status.2

Clinical Significance

Increased Protein

Increased protein (hyperproteinemia) may be associated with collagen vascular diseases (lupus, rheumatoid arthritis, scleroderma), sarcoidosis,
multiple myeloma, and dehydration.2

Decreased Protein

Decreased serum protein (hypoproteinemia) may result from a decreased ability to synthesize protein (liver disease) or an increased protein wasting
as seen in renal disease, nephrotic syndrome, and third­degree burns.2

Cholesterol
This test may or may not be a part of the blood chemistries panel. For a complete discussion of cholesterol, please see the section under cardiac tests.

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