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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2593_Библиотеки_им_академика_М_И_Перельмана
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interstitial glucose rather than capillary blood samples to estimate
plasma glucose levels.The accuracy of these monitors is believed to
lead to a clinically and statistically significant decline in both A1c and
hypoglycemia.
24
GLYCATED HEMOGLOBIN
Reference Range: 3.8%–6.4%
Hgb is the oxygen-carrying component of the red blood cell (RBC).
During the functional life span of RBCs (∼4 months), glucose
molecules irreversibly bind to Hgb, which results in glycated HgbA
1c
(A1c). The concentration of A1c reflects a patient’s average blood
glucose concentration for the life span of circulating RBCs. As a
result, measurement of A1c concentrations is useful to diagnose
diabetes, monitor disease progression, and/or assess the efficacy of
drug therapy. In a patient without diabetes, about 5% of Hgb is
glycated. To diagnose diabetes, two confirmatory A1c ≥6.5% are
needed.25 Of note, point-of-care (POC) A1c testing is generally not
recommended for diagnostic purposes because of concerns about
standardization and accuracy. Use of POC testing is limited to
assessment of glycemic control in the clinic setting.22 In situations
when the A1c is deemed unreliable because of changes in cell
turnover (eg, sickle cell anemia, hemodialysis, and pregnancy),
plasma glucose testing should be used for diagnosis.22 Both fasting
plasma glucose (FPG) and postprandial glucose contribute variably
to the A1c measurement. One study suggests that the higher the A
1c
(>8.5%), the greater the contribution of FPG to the A1c.26 As such,
the contribution of FPG decreases as the A1c decreases. The
American Diabetes Association suggests that an A1c of 7%
correlates to an estimated average glucose (eAG) of 154 mg/dL.
eAG can be calculated using the following equation: eAG (mg/dL) −
(28.7 − A1c) − 46.7.25 It has been estimated that for every 1%
reduction in A1c, the risk of microvascular complications is reduced
by 37% and the risk of acute myocardial infarction (MI) by 14%.
27
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HYPERGLYCEMIA AND HYPOGLYCEMIA
Hyperglycemia and hypoglycemia are nonspecific signs of abnormal
glucose metabolism. Diabetes mellitus is the most common cause of
hyperglycemia along with suboptimal use of insulin and/or other
antidiabetic agents, high carbohydrate dietary intake, physical
inactivity, recent illness or infection, and increased emotional stress.
Hyperglycemia may be caused or worsened by certain medications
such as corticosteroids, niacin (doses >2 g/day), thiazide and loop
diuretics, protease inhibitors, atypical antipsychotics, and 3-hydroxy3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors
(statins). Insufficient carbohydrate intake because of a missed meal
is the most common cause of hypoglycemia in a patient receiving
insulin or another hypoglycemic medication. In addition to insulin,
drug-induced hypoglycemia includes insulin secretagogues,
fluoroquinolone antibiotics, and select herbal products (eg, ginseng,
bitter melon, and cinnamon).
CASE 2-2
QUESTION 1: T.C., a 68-year-old male, visits his primary care provider to assess
control of his type 2 diabetes. His average blood sugar over the past 90 days
recorded by his blood glucose monitor is 195 mg/dL. However, T.C.’s A1c is 9%,
which correlates with an eAG of 240 mg/dL. T.C. is confused that these values
are different because he routinely ensures his blood glucose machine is
calibrated and coded properly.
Why is the laboratory average different?
T.C. should not be alarmed by the difference in these values. His
blood glucose monitor is likely working properly and adequately
measuring his plasma glucose concentrations. However, the monitor
may be reflecting a lower average glucose concentration because of
the timing of his daily testing for glucose. For example, measuring
blood glucose in a fasting state more frequently than after mealtime
could contribute to lower average concentrations because fasting
values are typically lower than are postprandial concentrations. The
A1c is more indicative of his average blood sugar control during the
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(Eq. 2-8)
past 90 days than the 90-day average recorded by his blood glucose
monitor.
Refer to Chapter 53, Diabetes Mellitus, for more detailed
information regarding glucose and HgbA1c.
Osmolality
Reference Range: 280–300 mOsm/kg or mmol/kg
The osmolality of a solution is a measure of the number of
osmotically active ions (ie, particles present) per unit of solution. It is
the total number of particles in the solution, not the weight of the
particle or the nature of the particle that determines osmolality.
Because 1 mole of a substance contains 6 × 1023 molecules,
equimolar concentrations of all substances in the undissociated state
exert the same osmotic pressure. A mole of an ionized compound
such as Na+Cl− contributes twice as many particles in solution as 1
mole of an undissociated compound such as glucose. In most
situations, the primary determinants of serum osmolality in the ECF
are sodium (and its accompanying anions), glucose, and BUN. If one
corrects for the concentrations of glucose and BUN, the serum
concentration of sodium closely mirrors the serum osmolality. A
useful formula (Eq. 2-8) is as follows:
Serum osmolality is helpful when evaluating fluid and electrolyte
disorders, particularly sodium imbalances. The difference between
the measured serum osmolality and the calculated serum osmolality
is commonly referred to as the osmol gap. Note that, in practice,
osmolality and osmolarity are often used interchangeably. The
reader is referred to Chapter 27, Fluid and Electrolyte Disorders, for
a more detailed discussion of osmolality.
MULTICHEMISTRY PANELS
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Frequently, multiple laboratory tests are needed for a given patient.
Common clinical laboratory panels include a basic metabolic panel
(BMP), comprehensive metabolic panel, electrolyte, hepatic function,
and renal function panels (Table 2-4). Clinicians will often use the
following abbreviated method to report a BMP in written medical
records:
Table 2-4
Common Multichemistry Panels
BMP, basic metabolic panel; BUN, blood urea nitrogen; CMP, comprehensive
metabolic panel; SGOT, serum glutamic:oxaloacetic transaminase; SGPT, serum
glutamic:pyruvic transaminase.
Multichemistry tests have become routinely used because they
quickly provide basic information concerning organ function at a
relatively low cost. In addition, laboratory automation frequently
makes it more cost effective to order a battery of tests within a panel
versus a single test. A potential disadvantage of obtaining a battery
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of tests, however, is that clinicians may be inclined to pursue further
laboratory testing when “abnormalities” are not clinically relevant. It
is important to note that the individual laboratory tests included in a
particular multichemistry panel may vary among clinical laboratories.
Calcium
Reference Range: 8.6–10.3 mg/dL or 2.2–2.74 mmol/L
Calcium has two key physiologic functions within our body; it is an
essential intracellular messenger in cells and tissues and a key
component of hydroxyapatite, which provides strength, rigidity, and
elasticity to the skeleton. All calcium in the body resides primarily in
the skeleton, with only about 1% freely exchangeable with that in the
ECF. This reservoir of calcium in bones maintains the concentration
of calcium in the plasma constant despite pronounced changes in
the external balance of calcium. If the homeostatic factors (ie,
parathyroid hormone, vitamin D, and calcitonin) that regulate the
calcium content of body fluid are intact, a patient can lose 25% to
30% of total body calcium without a change in the concentration of
calcium ions in the plasma. Alterations in serum calcium
concentrations may have a significant impact on a patient’s renal, GI,
and neurologic function. Hypercalcemia is associated with a
malignancy, use of thiazide diuretics, hyperthyroidism, and renal
failure. Hypocalcemia may indicate a presence of vitamin D
deficiency, hypothyroidism, rhabdomyolysis, and CKD.28 About 40%
of the calcium in the ECF is bound to plasma proteins (especially
albumin); 5% to 15% is complexed with phosphate and citrate; and
about 45% to 55% is in the unbound, ionized form. Most laboratories
measure the total calcium concentration; however, it is the free,
ionized calcium concentration that is important and closely regulated
physiologically. Most laboratories are also able to measure the
ionized form of calcium, which has a reference range of 4.5 to 5.6
mg/dL (1.13–1.4 mmol/L). Ionized calcium measures free calcium;
however, it is not routinely ordered.28 It is important to obtain an
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albumin level in patients to calculate a corrected calcium level that
would account for hypoalbuminemia.
CASE 2-3
QUESTION 1: P.M. is a 61-year-old male admitted status post (s/p) fall because
of alcohol intoxication. He has no known drug allergies. P.M.’s past medical
history is significant for alcohol-induced seizures, alcohol abuse × 20 years, and
hypertension. P.M.’s laboratory tests revealed the following:
Albumin: 2.0 g/dL
Ca: 6.8 mg/dL
Total bilirubin: 10.8 mg/dL
Serum aspartate aminotransferase (AST): 280 IU/L
Alkaline phosphatase: 240 IU/L
Would P.M. be considered hypocalcemic, and how should he be managed?
This case presentation provides insufficient patient data to make a
conclusion concerning treatment. However, it does illustrate the
importance of treating the patient as a whole, not as a specific
laboratory value. Because calcium in the serum is partially bound to
plasma proteins (mostly albumin), the serum calcium concentration
is affected by the concentration of these plasma proteins. If the
albumin concentration is low, the reported serum calcium will
generally be less than the lower limit of normal. A useful method to
estimate a corrected value for serum calcium in the presence of low
serum albumin is to use the following guideline: the total serum
calcium will decrease by 0.8 mg/dL for each decrease of 1.0 g/dL in
serum albumin concentration. Thus, evaluating P.M.’s corrected
calcium is indicated: (4 − albumin
patient
× 0.8) + calcium − corrected
calcium. For P.M., his “corrected” serum calcium is 8.4 mg/dL, which
is just below the reference range, and probably does not warrant
treatment with calcium supplementation unless his serum calcium
continues to decline. Direct measurement of ionized calcium is
independent of albumin concentration, making it unnecessary to
correct calcium concentrations in the presence of hypoalbuminemia.
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Unfortunately, some clinical laboratories do not have the capability of
measuring ionized calcium.
Magnesium
Reference Range: 1.3–2.2 mEq/L or 0.65–1.1 mmol/L
Magnesium is primarily an intracellular electrolyte principally stored
in bone and, together with potassium and calcium, helps maintain a
neutral charge within the cell. Magnesium also serves an important
metabolic role in the phosphorylation of adenosine triphosphate
(ATP). Magnesium is necessary for the formation of bone and teeth
and for normal nerve and muscle function.
A primary cause of hypomagnesemia is malnourishment. Some
other factors associated with hypomagnesemia are the use of
proton-pump inhibitors, chronic diarrhea, alcoholism, and diuretic
use. Toxemia in pregnancy is associated with hypomagnesemia.
Hypomagnesemia needs to be corrected before attempting to correct
hypokalemia or hypocalcemia. Attempts to replace potassium or
calcium in patients with hypomagnesemia will be ineffective until the
low magnesium concentrations are adequately addressed.
Excessive ingestion of magnesium-containing antacids can lead to
hypermagnesemia. Increased concentrations of magnesium are also
observed in patients with reduced renal function. Hypermagnesemia
can slow conduction in the heart, prolong PT intervals, and widen the
QRS complex.
Phosphate
Reference Range: 2.5–5 mg/dL or 0.80–1.6 mmol/L
The extracellular concentration of phosphate as inorganic
phosphorus is the prime determinant of the intracellular
concentration, which in turn is the source of phosphate for ATP and
phospholipid synthesis. Intracellular phosphate is also important in
the regulation of nucleotide degradation.
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The ECF concentration of phosphate is influenced by parathyroid
hormone, intestinal phosphate absorption, renal function, bone
metabolism, and nutrition. Moderate hypophosphatemia is
encountered by malnourished patients (especially when anabolism is
induced), patients who excessively use antacids (aluminumcontaining antacids bind phosphorus in the GI tract), chronic
alcoholics, and patients with sepsis. Clinical consequences of severe
hypophosphatemia involve nervous system dysfunction, muscle
weakness, rhabdomyolysis, cardiac irregularities, and dysfunction of
leukocytes and erythrocytes. Hyperphosphatemia is most commonly
caused by renal insufficiency, although increased vitamin D,
hypoparathyroidism, and advanced malignancies are also significant
causes.
Uric Acid
Reference Range: 3–8 mg/dL or 179–476 μmol/L
Uric acid is an end product of the metabolic breakdown of purines. It
is commonly referred to as a metabolically inert compound offering
little biologic utility. The renal system is responsible for 60% to 70%
of total body uric acid excretion. Most uric acid is freely filtered, with
~90% reabsorbed via the nephron.
Increased serum uric acid concentrations can result from either a
decrease in urate excretion (eg, renal dysfunction, competition with
drugs using the same transporters for elimination [thiazide diuretics,
niacin]) or excessive urate production (eg, increased purine
metabolism resulting from cytotoxic therapy of neoplastic or
myeloproliferative disorders). Gout, a common arthritic condition
characterized by hyperuricemia, is usually associated with increased
serum concentrations of uric acid along with deposits of
monosodium urate crystals in joints. Low serum uric acid
concentrations are inconsequential, and are usually reflective of
drugs that have hypouricemic activity (eg, high dosages of
salicylates).
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PROTEINS
Prealbumin
Reference Range: 19.5–35.8 mg/dL or 195–358 mg/L
Prealbumin is an important serum protein, but in comparison with
other proteins, it accounts for a relatively small percentage of all
circulating proteins. It is also referred to as thyroxine-binding
prealbumin owing to its role as a transport mechanism for
triiodothyronine (T3) and thyroxine (T4). However, it is most
frequently used to monitor patients at risk for poor nutrition (eg,
patients with eating disorders, patients with human
immunodeficiency virus, or patients receiving total parenteral
nutrition). Compared with the long half-life of albumin (about 3
weeks), the half-life of prealbumin is only 1 to 2 days. This shorter
half-life provides a more accurate reflection of acute changes in
protein synthesis, catabolism, and, ultimately, immediate nutrition
status. Hepatic disease and malnutrition are associated with
decreases in prealbumin (and albumin). Hodgkin lymphoma,
pregnancy, CKD, and corticosteroid use can increase prealbumin
serum concentrations.
Albumin
Reference Range: 3.6–5 g/dL or 36–50 g/L
Albumin, produced by the liver, contributes ~80% to serum colloid
osmotic pressure. As a result, hypoalbuminemic states are
commonly associated with edema and third spacing of ECF. A lack
of essential amino acids from malnutrition or malabsorption, or
impaired albumin synthesis by the liver, can result in decreased
serum albumin concentrations. Most forms of hepatic insufficiency
are associated with decreased synthesis of albumin. It can be lost
directly from the blood because of hemorrhage, burns, or exudates
or it may be lost directly into the urine because of nephrosis. Serum
albumin concentrations seldom increase, but increases may be
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noted in volume depletion, in shock, or immediately after the
administration of large amounts of IV albumin. In addition to its
diagnostic value, albumin concentration is an important
consideration in the therapeutic monitoring of drugs and electrolytes
that are highly protein bound (eg, phenytoin, digoxin, and calcium).
In cases of severe hypoalbuminemia, determination of the “free” or
unbound concentration of these entities might be necessary for an
accurate assessment of drug therapy.
Globulin
Reference Range: 2.3–3.5 g/dL or 23–35 g/L
In addition to albumin, globulin is another primary plasma protein.
Albumin principally functions to maintain serum oncotic pressure,
whereas globulins play an active role in immunologic processes. The
globulins can be separated into several subgroups such as α, β, and
γ. The γ-globulins can be separated further into various
immunoglobulins (Igs; eg, IgA, IgM, and IgG). Chronic infection or
rheumatoid arthritis can increase Ig levels, and fractionation of Igs
can provide useful information in the evaluation of immune disorders.
Because globulin is not manufactured solely by the liver, the ratio of
albumin to globulin (the A/G ratio) is changed in patients with liver
disease. Changes in this ratio result from decreased albumin
concentration and a compensatory increase in globulin
concentration.
CARDIAC MARKERS
Cardiac biomarkers are useful for the evaluation, diagnosis, and
monitoring of patients with suspected heart damage. These markers,
which include some enzymes, are often released into the blood
when the myocardium becomes damaged or dies. Enzyme activity is
typically expressed in terms of international units (IUs), where 1 IU is
the enzyme amount needed to catalyze the conversion of 1 μmol of
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