TRIPASS XR تري باس

 

1 Early elevation (within 3 hours) may

suggest myocardial injury, but less specific

than CK-MB or troponin

Homocysteine 4–12 μmol/L 4–12 μmol/L 1 Damages vessel endothelial, which may

increase the risk for cardiac disease.

Associated with deficiencies in folate,

vitamin B6

, and vitamin B12

LDH 100–250 IU/L 1.67–4.17

mkat/L

0.01667 High in heart, kidney, liver, and skeletal

muscle. Five isoenzymes: LD1 and LD2

mostly in heart, LD5 mostly in liver and

skeletal muscle, LD3 and LD4 are

nonspecific. ↑ in malignancy, extensive

burns, PE, renal disease

BNP <100 pg/mL <100 ng/L 1 BNP >500 ng/L indicates congestive heart

failure. Released from ventricles with ↑

workload placed on heart

NT-proBNP <60 pg/mL males

<150 pg/mL females

<60 ng/L

males

<150 ng/L

females

1 NT-proBNP has similar clinical utility to

BNP as a marker for CHF

CRP 0–1.6 mg/dL 0–16 mg/L 1 Nonspecific indicator of acute

inflammation. Similar to ESR, but more

rapid onset and greater elevation. CRP >3

mg/dL increases risk of cardiovascular

disease

hs-CRP 0–2.0 mg/L 0–2.0 mg/L 1 More sensitive measure of CRP;

concentrations from 0.5 to 10 mg/L; hsCRP <1.0 mg/L low risk for cardiovascular

disease; 1.0–3.0 mg/L average risk; and

>3.0 mg/L high risk for cardiovascular

disease

Liver Function

AST 0–35 units/L 0–0.58 μkat/L 0.01667 Large amounts in heart and liver; moderate

amounts in muscle, kidney, and pancreas. ↑

with MI and liver injury. Less liver specific

than ALT

ALT 0–35 units/L 0–0.58 μkat/L 0.01667 From heart, liver, muscle, kidney, pancreas.

↑ negligible unless parenchymal liver

disease. More liver specific than AST

ALP 20–130 units/L 0.33–2.17

μkat/L

0.01667 Large amounts in bile ducts, placenta, bone.

↑ in bile duct obstruction, obstructive liver

disease, rapid bone growth (e.g., Paget

disease), pregnancy

GGT Sensitive test reflecting hepatocellular

injury; not helpful in differentiating liver

disorders. Usually high in chronic alcoholics

Male 9–50 units/L

Female 8–40 units/L

Bilirubin—total 0.1–1 mg/dL 2–18 μmol/L 17.1 Breakdown product of hemoglobin, bound

to albumin, conjugated in liver. Total

bilirubin includes direct (conjugated) and

indirect bilirubin. ↑ with hemolysis,

cholestasis, liver injury

Bilirubin—

direct

0–0.2 mg/dL 0–4 μmol/L 17.1

Miscellaneous

Amylase 35–118 units/L 0.58–1.97

μkat/L

0.01667 Pancreatic enzyme; ↑ in pancreatitis or duct

obstruction

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p. 20

Lipase 10–160 units/L 0–2.67 μ kat/L 0.01667 Pancreatic enzyme, ↑ acute pancreatitis,

elevated for longer period than amylase

PSA 0–4 ng/mL 0–4 mcg/L 1 ↑ in BPH and also in prostate cancer. PSA

levels of 4–10 ng/mL should be worked up.

Risk of prostate cancer increased if free

PSA/total PSA <0.25

TSH 0.5–4.7 μ units/mL 0.5–4.7

munits/L

1 ↑ TSH in primary hypothyroidism requires

exogenous thyroid supplementation; ↓ TSH

in hyperthyroidism

Procalcitonin <0.5 ng/mL <0.5 mcg/L 1 ↑ Bacterial infections—low risk of sepsis if

<0.5 ng/mL; high risk of severe sepsis if

>2.0 ng/mL

Total

cholesterol

<200 mg/dL <5.2 mmol/L 0.02586 Current guidelines do not recommend a

target level; consult current guidelines

LDL <100 mg/dL <2.58 mmol/L 0.02586 Current guidelines do not recommend a

target level, but rather starting moderate- to

high-intensity statin therapy based on

current risk factors; consult current

guidelines

HDL Female: >50 mg/dL Female: >1.29 0.02586 Current guidelines do not recommend a

Male: >40 mg/dL mmol/L

Male: >1.03

mmol/L

target level; consult current guidelines

Triglycerides

(fasting)

<150 mg/dL <1.70 mmol/L 0.0113 ↑ by alcohol, saturated fats, drugs. Obtain

fasting level. Current guidelines do not

recommend a target level

ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; BNP, brain

natriuretic peptide; BPH, benign prostatic hypertrophy; BUN, blood urea nitrogen; CHF, congestive heart failure;

CK, creatine kinase (formerly known as creatine phosphokinase); CrCl, creatinine clearance; CRP, C-reactive

protein; cTnI, cardiac troponin I; ESR, erythrocyte sedimentation rate; GFR, glomerular filtration rate; GGT, γglutamyl transferase; GI, gastrointestinal; HDL, high-density lipoprotein; IM, intramuscularly; LDH, lactate

dehydrogenase; LDL, low-density lipoprotein; MI, myocardial infarction; NG, nasogastric; PE, pulmonary

embolism; PSA, prostate-specific antigen; SI, International System of Units; TPN, total parenteral nutrition; TSH,

thyroid-stimulating hormone.

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p. 21

Table 2-3

Hematologic Laboratory Values

Laboratory Test

Normal Reference Values

Comments

Conventional

Units SI Units

RBC count

Male 4.3–5.9 × 10

6

/μL 4.3–5.9 × 10

12

/L

Female 3.5–5.0 × 10

6

/μL 3.5–5.0 × 10

12

/L

Hct ↓ with anemias, bleeding, hemolysis. ↑ with

polycythemia, chronic hypoxia

Male 40.7%–50.3% 0.4–0.503

Female 36%–44.6% 0.36–0.446

Hgb Similar to Hct

Male 13.8–17.5 g/dL 138–175 g/L

Female 12.1–15.3 g/dL 121–153 g/L

MCV 80–97.6 μ m

3 80–97.6 fL

a Describes average RBC size; ↑ MCV =

macrocytic, ↓ MCV = microcytic

MCH 27–33 pg 1.66–2.09 fmol/cell Measures average weight of Hgb in RBC

MCHC 33–36 g/dL 20.3–22 mmol/L More reliable index of RBC hemoglobin

than MCH. Measures average

concentration of Hgb in RBC.

Concentration will not change with weight

or size of RBC

Reticulocyte count

(adults)

0.5%–1.5% 0.005–0.015 Indicator of RBC production; ↑ suggests ↑

number of immature erythrocytes released

in response to stimulus (e.g., iron in irondeficiency anemia)

ESR 0–30 mm/hour 0–30 mm/hour Nonspecific; ↑ with inflammation, infection,

neoplasms, connective tissue disorders,

pregnancy, nephritis. Useful monitor of

temporal arteritis and polymyalgia

rheumatica

WBC count 3.8–9.8 × 10

3

/μ L 3.8–9.8 × 10

9

/L Consists of neutrophils, lymphocytes,

monocytes, eosinophils, and basophils; ↑ in

infection and stress

ANC 2,000 cells/μ L ANC = WBC × (% neutrophils +%

bands)/100; if <500 ↑ risk infection, if

>1,000 ↓ risk infection

Neutrophils 40%–70% 0.4–0.7 ↑ in neutrophils suggests bacterial or fungal

infection. ↑ in bands suggests bacterial

infection

Bands 0%–10% 0–0.1

Lymphocytes 22%–44% 0.22–0.44

Monocytes 4%–11% 0.04–0.11

Eosinophils 0%–8% 0–0.08 Eosinophils ↑ with allergies, parasitic

infections, and certain neoplasms

Basophils 0%–3% 0–0.03

Platelets 150–450 × 10

3

/μ L 150–450 × 10

9

/L <100 × 10

3

/μ L = thrombocytopenia; <20 ×

10

3

/μ L = ↑ risk for severe bleeding

Iron

Male 45–160 mcg/dL 8.1–31.3 μ mol/L Body stores two-thirds in Hgb; one-third in

bone marrow, spleen, liver; only small

amount present in plasma. Blood loss major

cause of deficiency

Female 30–160 mcg/dL 5.4–31.3 μ mol/L ↑ needs in pregnancy and lactation

TIBC 220–420 mcg/dL 39.4–75.2 μ mol/L ↑ capacity to bind iron with iron deficiency

ANC, absolute neutrophil count; ESR, erythrocyte sedimentation rate; Hct, hematocrit; Hgb, hemoglobin; MCH,

mean corpuscular hemoglobin; MCHC, mean cell hemoglobin concentration; MCV, mean cell volume; RBC, red

blood cell; SI, International System of Units; TIBC, total iron-binding capacity; WBC, white blood cell.

a

fL, femtoliter; femto, 10

−15

; pico, 10

−12

; nano, 10

−9

; micro, 10

−6

; milli, 10

−3

.

FLUIDS AND ELECTROLYTES

Please refer to Chapter 27, Fluid and Electrolyte Disorders, for more detailed

information.

Sodium

Reference Range: 135–147 mEq/L or mmol/L

Sodium is the predominant cation of the extracellular fluid (ECF), and human cells

reside in salt water. Along with chloride, potassium, and water, sodium is important

in establishing serum osmolarity and osmotic pressure relationships between

intracellular fluid (ICF) and ECF. Osmoregulatory system regulates the plasma

sodium concentrations to remain in a normal range by controlling water intake and

excretion.

6 An increase in the serum sodium concentration could suggest either

impaired sodium excretion or volume contraction. On the contrary, a decrease in the

serum sodium concentration to less-than-normal values could reflect hypervolemia,

abnormal sodium losses, or sodium starvation. Although healthy individuals are able

to maintain sodium homeostasis without difficulty, patients with kidney failure, heart

failure, or lung disease often encounter sodium and water imbalances. In adults,

changes in serum sodium concentrations most often represent water rather than

sodium imbalance. Therefore, serum sodium concentrations are more reflective of a

patient’s fluid status rather than sodium balance. Clinical manifestations of

hyponatremia or hypernatremia are mostly neurologic, and rapid changes in serum

sodium concentrations can lead to severe and sometimes fatal brain injury.

6

HYPONATREMIA

Hyponatremia can result from dilution of the sodium concentration in serum or from a

total body depletion of sodium. The finding of hyponatremia implies that sodium has

been diluted throughout all body fluids because water moves freely across cell

membranes in response to oncotic pressures. Hyponatremia can denote low, high, or

normal tonicity. Dilutional hyponatremia is the most common form and results from

water retention.

7 Some clinical conditions such as cirrhosis, congestive heart failure

(CHF),

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p. 22

the syndrome of inappropriate antidiuretic hormone secretion (SIADH), and renal

impairment, as well as the administration of osmotically active solutes (e.g., albumin

and mannitol) are commonly associated with dilutional hyponatremia. Drugs that can

induce SIADH, thereby causing a reversible hyponatremia (especially in the elderly),

include cyclophosphamide, carbamazepine, desmopressin, oxcarbazepine, oxytocin,

serotonin selective reuptake inhibitors, and vincristine.

7,8 Hyponatremia that results

from sodium depletion presents as a low serum sodium concentration in the absence

of edema. Sodium-depletion hyponatremia can be caused by mineralocorticoid

deficiencies, sodium-wasting renal disease, or replacement of sodium-containing

fluid losses with nonsaline solutions.

7 Therapy with thiazide diuretics may also lead

to the development of severe hyponatremia. Hyponatremia can be frequently seen in

hospitalized patients; however, morbidity varies significantly in severity, and serious

complications can be due to the disorder itself or due to the inappropriate

management and rapid correction of the sodium levels.

HYPERNATREMIA

Hypernatremia represents a state of relative water deficiency in relation to the

body’s sodium stores. Because sodium contributes to the cell’s tonicity,

hypernatremia denotes hypertonicity and at least transient cellular dehydration.

9

Some of the causes of hypernatremia are loss of free water, loss of hypotonic fluid,

or excessive sodium intake. Free water loss is uncommon, except in the presence of

diabetes insipidus. Diarrhea is the most common cause of hypotonic fluid loss in

infants and the elderly. Increased retention of sodium in patients with

hyperaldosteronism can also increase serum sodium concentrations. Excessive salt

intoxication is usually accidental or iatrogenic and most commonly results from

inappropriate intravenous administration of hypertonic salt solutions. Some β-lactam

antibiotics (e.g., ticarcillin) contain a modest sodium load and can cause fluid

overload when high dosages are administered.

The primary defense against hypertonicity is thirst and subsequent fluid intake.

Hypernatremic syndromes, therefore, usually occur in patients who are unable to

drink sufficient fluids. For example, demented elderly patients are at increased risk

because they depend on others for their water requirements. Similarly, patients who

are vomiting, comatose, or not allowed oral fluids are at risk for hypernatremia.

Potassium

Reference Range: 3.5–5.0 mEq/L or mmol/L

Potassium is the most abundant intracellular cation in the body responsible for

regulating enzymatic function and neuromuscular tissue excitability. Approximately

90% of the total body potassium is found in the ICF, with the majority in muscle, and

only about 10% available in the ECF. The potassium ion in the ECF is filtered freely

at the glomerulus of the kidney, reabsorbed in the proximal tubule, and secreted into

the distal segments of the nephron. Because the majority of potassium is sequestered

within cells, a serum potassium concentration is not a good measure of total body

potassium. Intracellular potassium, however, cannot be measured easily. Fortunately,

the clinical manifestations of potassium deficiency (e.g., fatigue, drowsiness,

dizziness, confusion, electrocardiographic changes, muscle weakness, and muscle

pain) correlate well with serum concentrations. The serum potassium concentration

is buffered and can be within normal limits despite abnormalities in total body

potassium. During potassium depletion, potassium moves from the ICF into the ECF

to maintain the serum concentration. When the serum concentration decreases by a

mere 0.3 mEq/L, the total body potassium deficit is approximately 100 mEq. Serum

potassium concentrations, therefore, can be misleading when interpreted in isolation

from other considerations, and assumptions should not be made as to the status of

total body potassium concentration based solely on a serum concentration

measurement. Disorders of potassium are commonly the result of (1) alterations in

intake, (2) alterations with excretion, and/or (3) unbalanced transcellular shifting of

potassium (e.g., metabolic acidosis/alkalosis).

HYPOKALEMIA

The kidneys are responsible for about 90% of daily potassium loss (~40–90

mEq/day), and the remaining 10% of potassium is excreted in the stool and a

negligible amount in sweat. The kidneys, however, have only a limited ability to

conserve potassium. Even when potassium intake has ceased, the urine will contain

at least 5 to 20 mEq of potassium per 24 hours. Therefore, prolonged intravenous

therapy with potassium-free solutions in a patient unable to obtain potassium in foods

(e.g., nothing by mouth) can result in hypokalemia. Hypokalemia can also be induced

by osmotic diuresis (e.g., mannitol and glucosuria), use of thiazide or loop diuretics

(e.g., hydrochlorothiazide, furosemide, respectively), excessive mineralocorticoid

activity, or protracted vomiting. Although the fluid secreted along most of the upper

gastrointestinal (GI) tract contains only a modest amount of potassium (i.e., 5–20

mEq/L), vomiting can induce hypokalemia because of the combined effect from

decreased food intake, loss of acid, alkalosis, and loss of sodium. The loss of large

amounts of colonic fluid through severe diarrhea and/or laxative abuse can cause

potassium depletion because fluid in the colon is high in potassium content (i.e., 30–

40 mEq/L). Insulin and stimulation of β2

-adrenergic receptors can also induce

hypokalemia because both increase the movement of potassium into cells from the

ECF. The magnitude of a potassium deficiency is difficult to establish because of the

limited presence of potassium in the ECF. Equation 2-1 can be used to estimate the

potassium deficit with hypokalemia:

It is also important to note that hypomagnesemia often accompanies hypokalemia,

because magnesium is necessary for the shifting of sodium, potassium, and calcium in

and out of cells. As a result, hypokalemic individuals not responding to potassium

therapy may be refractory to treatment until hypomagnesemia is corrected. Some

laboratories omit magnesium from the general electrolyte panel, so this test may need

to be specially ordered.

HYPERKALEMIA

Hyperkalemia most commonly results from decreased renal excretion of potassium

(e.g., renal failure, renal hypoperfusion, and hypoaldosteronism), excessive

exogenous potassium administration, or excessive cellular breakdown (e.g.,

hemolysis, burns, crush injuries, surgery, and infections). Drug-induced causes

include angiotensin converting enzyme inhibitors, angiotensin receptor blockers,

aldosterone antagonists, and nonsteroidal antiinflammatory drugs, to name a few.

Metabolic acidosis can also induce hyperkalemia because hydrogen ions move into

cells in exchange for potassium and sodium. Abnormal potassium concentrations in

the serum primarily affect excitability of nerve and muscle tissue (e.g., myocardial

tissue). As a result, arrhythmias can be induced by hyperkalemia or hypokalemia.

Potassium also affects some enzyme systems and acid–base balance, as well as

carbohydrate and protein metabolism.

Carbon Dioxide Content

Reference Range: 21–32 mEq/L or mmol/L

p. 22

p. 23

The carbon dioxide (CO2

) content in the serum represents the sum of bicarbonate

(HCO3

) and dissolved CO2 concentrations. The dissolved CO2

represents a

relatively small component of total CO2 content, making CO2 essentially a measure of

the serum bicarbonate. Chloride and bicarbonate are the primary negatively charged

anions that offset the positively charged cations (i.e., sodium and potassium).

Although several buffer systems (e.g., hemoglobin [Hgb], phosphate, and protein)

participate in regulating pH within physiologic limits, the carbonic acid–bicarbonate

system is the most important. From a clinical standpoint, most disturbances of acid–

base balance result from imbalances of the carbonic acid–bicarbonate system. The

importance of bicarbonate in maintaining physiologic pH is presented in Chapter 26,

Acid–Base Disorders.

Chloride

Reference Range: 95–110 mEq/L or mmol/L

Chloride (Cl

−