Complete Chemistry Profile
Glucose
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Formed from carbohydrate digestion and
conversion of glycogen to glucose by the
liver.
Regulated by glucagon and insulin.
Glucagon accelerates glycogen breakdown
in the liver and increases blood glucose
level.
Insulin increases cell membrane
permeability to glucose, and transports
glucose into cells.
Glucose
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Insulin binds to insulin receptors on the
surface of target cells found in fat and
muscle.
Opens channels so that glucose can
pass into cells where it can be
converted to energy.
ACTH, adrenocorticosteroids,
epinephrine, and thyroxine play key
roles in glucose metabolism.
Glucose
Hyperglycemia
 Diabetes
 Drugs: Steroids,
epinephrine,
amphetamines, thiazides
 Critical illness
Hypoglycemia
 Reactive postpandrial, or
fasting
 Insulin mediated or
insulinoma
 Pseudohypoglycemia
(Laboratory)
 Factitious (Non
therapeutic adm of
sulfonylureas or insulin)
Sodium
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Cation 90% of the electrolyte fluid.
Chief base of the blood.
Chemically maintains osmotic pressure and
acid base balance to transmit nerve
impulses.
Mechanisms to maintain Na+ levels in
plasma and extracellular fluid include renal
blood flow, carbonic anhydrase enzyme
activity, aldosterone, renin enzyme
secretion, ADH, and vasopressin secretion.
Potassium
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Principle cation of intracellular fluid.
Primary buffer within the cell.
90% concentrated within the cell, when
damaged cells release K+ into the
blood.
80-90% excreted in the urine by the
glomeruli. Kidneys do not conserve K+.
Average daily consumption is 80-200
mEq/day.
Potassium
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Facilitates nerve conduction, muscle
function, acid base balance, and osmotic
pressure.
Controls rate and force of contraction of the
heart, CO.
K+ and Na+ ions are important in renal
regulation of acid base balance as hydrogen
ions are substituted for Na+ and K+ions in
the renal tubule.
Potassium
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K+ Deficiency causes intracellular increase
bicarbonate causing the pH to be alkaline.
The respiratory center responds by
increasing PC02 through hypoventilation.
K+ concentration is affected by adrenal
hormones.
K+ deficiency causes a significant reduction
in protein synthesis.
Hyperkalemia
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Increase K intake (Diet, Blood
transfusion, TPN)
K movement out of the cell (b blocker,
Rjabdomyolysis, Burns, Tumor lysis
syndrome, metabolic acidosis
Decrease k excretion (ACEI, K sparing
diuretics, NSAIDs
Hypoaldosteronism
Renal insufficiency
Hypokalemia
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GI loss
Intracellular shift (albuterol, excessive
beta stimulation, hyperthyroidism,
insulin)
Renal losses (diuretics, adrenal steroid
excess)
Chloride
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Anion that exists in the extracellular
spaces.
Maintains cellular integrity through
osmotic pressure, acid base and water
balance
Excreted with cations during massive
diuresis.
Diagnoses disorders of acid base and
water balance.
CO2
Lower-than-normal levels
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Addison disease
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Diarrhea
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Ethylene glycol poisoning
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Ketoacidosis
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Kidney disease
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Lactic acidosis
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Metabolic acidosis
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Methanol poisoning
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Salicylate toxicity (such as aspirin overdose)
Higher-than-normal levels
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Breathing disorders
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Cushing syndrome
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Hyperaldosteronism
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Vomiting
The following conditions may also alter bicarbonate levels:
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Alkalosis
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Delirium
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Dementia
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Renal tubular acidosis; distal
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Renal tubular acidosis; proximal
Calcium
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Bulk of Ca+ stored in the skeleton and teeth
98-99%
50% of blood calcium is ionized
50% is protein bound
Only ionized calcium can be used by the
body for muscular contraction, cardiac
function, transmission of nerve impulses and
blood clotting.
Test measures concentration of total and
ionized calcium in blood and reflects
parathyroid function, calcium metabolism
and malignancy activity.
Phosphate
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85% is combined with calcium in the
bone
15% remains within the cells
Required for generation of bony tissue
and functions in the metabolism of
glucose and lipids, the maintenance of
acid base balance and the transfer of
energy from one site in the body to
another.
Phosphate
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Phosphorus enters the RBC with
glucose.
Levels are evaluated in relation to CA+
levels. There is an inverse relationship.
Decreased phosphorus may be due to
elevated calcium levels.
Controlling factor is PTH
Magnesium
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Concentrated in the bone, cartilage and
within the cell.
Required for the use of adenosine
triphosphate (ADP)
Necessary for carbohydrate metabolism
Protein synthesis
Nucleic acid synthesis
Contraction of muscular tissue
Magnesium
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Regulates neuromuscular irritability and
clotting mechanism.
Importance in absorption of calcium from
intestines.
Deficiency results in Ca+ coming out of the
bones and causing abnormal calcification in
the aorta and kidney.
95% of magnesium is filtered through the
glomerulus and reabsorbed in the tubule.
Blood Urea Nitrogen
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Urea forms in the liver along with CO2,
constitutes the final product of protein
metabolism.
Excreted urea is dependant on dietary protein
intake, increased excretion in fever, diabetes
and increased adrenal gland activity.
Measures the nitrogen portion of urea.
Index of glomerular function in the production
and excretion of urea.
Increased BUN indicates protein catabolism,
kidney impairment, severe impaired glomerular
function.
Creatinine
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Byproduct in the breakdown of muscle
creatine phosphate as a result of energy
metabolism.
Removed from the body by the kidneys.
Production of creatinine is constant as long
as muscle mass remains constant.
Decreased kidney function reduces
excretion of creatinine.
Diagnoses impaired renal function.
BUN/Creatinine
Increased blood urea nitrogen (BUN) may be
due:
 prerenal causes (cardiac decompensation,
water depletion due to decreased intake and
excessive loss, increased protein catabolism,
and high protein diet)
 renal causes (acute glomerulonephritis,
chronic nephritis, polycystic kidney disease,
nephrosclerosis, and tubular necrosis)
 postrenal causes (eg, all types of obstruction
of the urinary tract, such as stones, enlarged
prostate gland, tumors).
Serum Osmolality
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Measure of number of dissolved solute
particles in solution.
Increases with dehydration.
Decreases with fluid overload.
Evaluates water and electrolyte
balance.
Assesses liver disease, ADH function,
ethanol and ethylene glycol and
methanol ingestions.
Amylase & Lipase
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Amylase enzyme that changes starch
to sugar.
Produced in salivary glands, pancreas,
liver, fallopian tubes.
Lipase changes fats to fatty acids and
glycerol.
Pancreas is major source of lipase.
Diagnose acute pancreatitis.
Bilirubin
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Results from the breakdown of
hemoglobin in RBCs and is a
byproduct of hemolysis.
Produced by reticuloendothelial
system.
Removed by the liver, excretes it into
bile.
Level is elevated when there is
excessive destruction of RBCs or when
the liver is unable to excrete bilirubin.
Uric Acid
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Formed from the breakdown of
nucleonic acids.
End product of purine metabolism.
Excreted by urine and stool.
Overproduction occurs during
excessive cell breakdown and
catabolism of nucleonic acids.
Used to evaluate renal failure, gout,
and leukemia.