Lab Values BLOOD

Alanine Aminotransfrase

Adult/child: 4-36 units/L (SI units)1

Elderly: may be slightly higher than adult values

• Hepatitis
• Hepatic Necrosis
• Hepatic Ischemia

• • Cirrhosis
• • Hepatic tumor
• • Cholestasis (obstructive jaundice)
• • Hepatotoxic drugs
• • Severe burns

• • Myositis
• • Pancreatitis
• • Myocardial infarction
• • Infectious mononucleosis
• • Shock: injury or disease affecting the liver, heart, or muscles will cause a release of this
• enzyme into the bloodstream.

Alkaline Phosphatase (ALP or ALK Phos)

• Elderly: slightly higher than adult
• Adult: 30 120 units/L

These values are used to identify hepatocellular diseases of the liver. It is also an accurate monitor of improvement or worsening of these diseases.

These values may be used to detect and monitor diseases of the liver or bone.

• • Primary cirrhosis
• • Intrahepatic or extrahepatic biliary obstruction
• • Primary or metastatic liver tumor
• • Normal pregnancy (third trimester, early postpartum period)
• • Normal bones of growing children
• • Metastatic tumor to the bone
• • Healing fracture
• • Hyperparathyroidism
• • Paget disease
• • Rheumatoid arthritis
• • Intestinal ischemia or infarction
• • Myocardial Infarction

• • Malnutrition
• • Milk-alkali syndrome
• • Pernicious anemia
• • Scurvy (vitamin C deficiency)

• • Recent ingestion of a meal can increase the ALK Ph level
• • Age: young children with rapid bone growth. This is magnified during the growth spurt.
• • Drugs that may cause increased ALK Ph levels (ie: albumin made from placental tissues,
• allopurinol, antibiotics, methyldopa, tetracycline)

Ammonia

• Normal Findings:
• Adults: 15-60 micrograms per deciliter (mcg/dL) or
• 21-50 micromoles per liter (mcmol/L)

Ammonia is used to support the diagnosis of severe liver diseases, and for surveillance of these diseases. Ammonia levels are also used in the diagnosis and follow-up of hepatic encephalopathy.

Ammonia is a by-product of the breakdown of protein. Most ammonia in the body forms when protein is broken down by bacteria in the intestinal tract. By way of the portal vein it goes to the liver, where it is normally converted into urea and then secreted by the kidneys. Impaired renal function diminishes excretion of ammonia and the blood levels rise. High levels of ammonia in the liver may be caused by diseases of the liver (Cirrhosis or severe hepatitis). Ammonia then crosses the blood/brain barrier and could result in encephalopathy or neurological dysfunction.

• • Hemolysis increases ammonia levels because the RBCs have about three times the ammonia level content of plasma.
• • Muscular exertion can increase ammonia levels.
• • Cigarette smoking can produce significant increases in ammonia levels within 1 hour of
• inhalation.
• • Drugs that may cause increased ammonia levels include acetazolamide, alcohol,
• barbiturates, narcotics, parenteral nutrition and diuretics (loop, thiazide).
• • Drugs that may cause decreased ammonia levels include broad-spectrum antibiotics (neomysin), lactulose, levodopa, lactobacillus, and potassium salts.

• • Primary hepatocellular disease
• • Reyes Syndrome
• • Portal Hypertension
• • Severe heart failure with congestive hepatomegaly:
• The portal blood flow from the gut to the liver is altered. The ammonia cannot get to the liver to be metabolized for excretion. Furthermore the ammonia from the gut is rapidly shunted around the liver (by way of gastroesophageal varices) and into the systemic circulation.
• • GI bleeding with mild liver disease
• • GI obstruction with mild liver disease:
• Ammonia production is increased because the bacteria have more protein (blood) to catabolize. An impaired liver may not be able to keep up with the increased load of ammonia presented to it.

• • Essential or malignant hypertension
• • Hyperornithinemia

Lipase

Normal Findings: Adult: < 100 u/L

To detect and monitor the clinical course of pancreatitis.

When a patient complains of acute abdominal pain

The serum amylase test, which is easy and rapidly performed, is most specific for pancreatitis. Amylase is normally secreted from pancreatic acinar cells into the pancreatic duct and then into the duodenum. Once in the intestine it aides in the breakdown of carbohydrates (starch) to their component simple sugars. Damage to pancreatic acinar cells (as in pancreatitis) or obstruction of the pancreatic duct flow (as in pancreatic carcinoma or common bile duct gallstones) causes an outpouring of this enzyme into the intrapancreatic lymph system and the free peritoneum.

• IV dextrose solutions can lower amylase levels and cause a false-negative result.

• Drugs that may cause increased serum amylase levels include aminosalicylic acid, aspirin, azathioprine, corticosteroids, dexamethasone, ethyl alcohol, glucocorticoids, loop diuretics (eg: furosemide), methyldopa, narcotic analgesics, oral contraceptives and prednisone.

• Drugs that may cause decreased levels include citrates, glucose and oxalates.

• Acute pancreatitis

• Chronic relapsing pancreatitis:

Damage to pancreatic acinar cells as in pancreatitis causes an outpouring of amylase into the intrapancreatic lymph system and the free peritoneum. Blood vessels draining the free peritoneum and absorbing the lymph pick up the excess amylase.

• Penetrating peptic ulcer into the pancreas:

The peptic ulcer penetrates the posterior wall of the duodenum into the pancreas. This causes a localized pancreatitis with elevated amylase levels.

• GI disease:

In patients with perforated peptic ulcer, necrotic bowel, perforated bowel, or duodenal obstruction, amylase leaks out of the gut and into the free peritoneal cavity.

• Acute cholecystitis

• Parotiditis (mumps)

• Renal failure Amylase is cleared by the kidney. Renal diseases will reduce excretion of amylase.

• Diabetic Ketoacidosis

• Pulmonary infarction

BUN : Blood Urea Nitrogen Serum

2-9 mole/L

Would indicate serious impairment of renal function.

Urea (BUN) is an indirect and rough measurement of renal function and glomerular filtration rate (if normal liver function exists). It is also a measurement of liver function. It is performed on patients undergoing routine laboratory testing. It is usually performed as a part of a multiphase automated testing process.

The Urea measures the amount of urea nitrogen in the blood. Urea is formed in the liver as the end product of protein metabolism and digestion. During ingestion, protein is broken down into amino acids. In the liver these amino acids are broken down and free ammonia is formed. The ammonia molecules are combined to form urea, which is then deposited in the blood and transported to the kidneys for excretion. Therefore the Urea is directly related to the metabolic function of the liver and the excretory function of the kidney. It serves as an index of the function of these organs.

Nearly all renal diseases cause an inadequate excretion of urea, which causes the blood concentration to rise above normal. The Urea is interpreted in conjunction with the creatinine test. These tests are referred to as “renal function studies”. The Urea is less accurate than creatinine as an indicator of renal disease.

• Shock

• Burns

• Dehydration:

With reduced blood volume, renal blood flow is diminished. Therefore renal excretion of Urea is decreased and Urea levels rise.

• Congestive Heart Failure

• Myocardial Infarction With reduced cardiac function, renal blood flow is diminished. Therefore renal excretion of urea is decreased and urea levels rise.

• GI bleeding

• Starvation As protein is broken down to amino acids at an accelerated rate, urea is formed at a higher rate and urea accumulates.

• Sepsis As sepsis increases in severity, renal blood flow and primary renal function are reduced due to hypoperfusion. Urea levels rise.

• Liver failure:

Urea is made in the liver from urea. Reduced liver function is associated with reduced urea levels.

Brain Natriuretic Peptide

BNP < 100 pg/mL

Used to identify and stratify patients with congestive heart failure.

ANP —is synthesized in the cardiac atrial muscle

BNP —the main source of BNP in the cardiac ventricle

C-type — is produced by the endothelial cells

22-77 pg/mL

They are neuroendocrine peptides that prevent the activity of the renin-angiotensin system.

A complex biological system between the heart, brain, blood vessels, and kidneys that leads to the production of biologically active agents including angiotensin I and II and aldosterone.

Meaning literally “blood movement.” Which is the study of blood flow or the circulation.

are continuously released by the heart muscle cells in low levels. The rate of release can be increased by a variety of physiological factors including hemodynamic load 5 to regulate cardiac reload and afterload.

• ▪️Hypertension
• ▪️CHF
• ◾️atherosclerosis

Both BNP and ANP are released in response to atrial and ventricular stretch causing vasorelaxation, inhibition of aldosterone secretion from the adrenal gland and renin from the kidney, resulting in increasing the natriuresis and reduction in blood volume.

BNP correlates to the left ventricular pressures so is a good indicator for CHF. The increasing levels of BNP the more severe the CHF. This test is becoming increasingly used in urgent care settings to aid in the differential diagnosis of shortness of breath (SOB). 6 If the BNP is elevated, the SOB is related to CHF. If BNP levels are normal then SOB is pulmonary and not cardiac in nature. This is particularly useful in assessing patients with medical histories of both cardiac and chronic lung disease.

• BNP levels are generally higher in healthy women than healthy men

• BNP levels are higher in older patients

• Congestive Heart Failure

• Myocardial infarction

• Systemic hypertension

98-108 mmol/L

Chloride is the major extracellular anion. It’s primary purpose is to maintain electrical neutrality. This test is performed as a part of multiphase testing for what is usually called “electrolytes”. By itself, this test does not provide much information. However, with interpretation of the other electrolytes, chloride can give an indication of acid-base balance and hydration status.

May include: lethargy, weakness and deep breathing.

hyperexcitability of the nervous system and muscles, shallow breathing, hypotension and tetany.

• Excessive infusions of saline solutions can results in increased chloride levels.

• Drugs that may cause increased serum chloride levels include androgens, chlorothiazide, cortisone preparations, estrogens, hydrochlorothiazide, methyldopa, and nonsteroidal antiinflammatory.

• Drugs that may cause decreased levels include aldosterone, bicarbonates, corticosteroids, cortisone, hydrocortisone, loop diuretics, thiazide diuretics and triamterene.

• Dehydration Chloride ions are more concentrated in the blood.

• Excessive infusion of normal saline solution Intake of chloride exceeds output, and blood levels rise.

• Kidney dysfunction

• Over-hydration

• Congestive heart failure Chloride is retained with sodium retention but is diluted by excess total body water.

• Vomiting or prolonged gastric suction

• Chronic diarrhea Chloride is high in the stomach and GI tract because of HCl acid produced in the stomach.

• Chronic respiratory acidosis

• Burns Sodium and Chloride losses from massive burns can be great.

Adult: < 165 U/L

This test is used to support the diagnosis of myocardial muscle injury (Infarction). It can also indicate neurologic or skeletal muscle diseases.

CK is found predominantly in the heart muscle, skeletal muscle, and brain. Serum CK levels are elevated when these muscle or nerve cells are injured. CK levels can rise within 6 hours after damage. If damage is not persistent, the levels peak at 18 hours after injury and return to normal in 2 to 3 days. When the total CK level is elevated injury to or disease of the skeletal muscle is present. Examples of this include myopathies, vigorous exercise, multiple intramuscular (IM) injections, ETC, cardioversion, chronic alcoholism, or surgery. Because CK is made only in the skeletal muscle, the normal value of total CK varies according to a person’s muscle mass. Large muscular people may normally have a CK level in the high range of normal. This is important because high normal CK levels in these patients can mask a MI.

Creatine Kinase (CK) (aka Troponins)

Because its blood clearance and metabolism are well known, its frequent determination (on admission and at 12 hours & 24 hours) can accurately reflect timing, quantity, and resolution of a MI. New blood assays for cardiac markers have promised to rapidly and accurately detect acute MI in the emergency room.

4-6 hours following an MI.

4

• ▪️Total CK
• ▪️CK
• ▪️Troponin T
• ▪️Troponin I

24 hours following an MI

18 hours following an MI

10-24 hours following an MI

10-24 hours following an MI

3-4 days following an MI

2 days following an MI

10 days following an MI

4 days following an MI

• IM injections can cause elevated CK levels

• Strenuous exercise and recent surgery may cause increased levels

• Muscle mass is directly related to a patient’s normal CK level

• Drugs that may cause increased levels include ampicillin, some anesthetics, anticoagulants, aspirin, dexamethasone (Decadron), furosemide (Lasix), captopril, alcohol, lovastatin, lithium, lidocaine, propranolol, and morphine.

• Diseases or injury affecting the heart muscle, skeletal muscle, and brain

• AMI

• Cardiac aneurysm surgery

• Cardiac defibrillation

• Myocarditis

• Ventricular arrhythmias

• Cardiac ischemia

Any disease or injury to the myocardium causes CK-MB to spill out of the damaged cells and into the bloodstream, producing elevated CK-MB isoenzyme levels.

Adult: 45-110 umol/L

Creatinine is as part of a complete renal function panel including Urea and the eGFR which will be calculated to assist in the diagnosis of impaired renal function.

Creatinine is a catabolic product of creatine phosphate, which is used in skeletal muscle contraction. The daily production of creatine, and subsequently creatinine, depends on muscle mass, which fluctuates very little. Creatinine, as Urea is excreted entirely by the kidneys and therefore is directly proportional to renal excretory function.

Thus, with normal renal excretory function, the serum creatinine level should remain constant and normal.

• Renal disorders would cause an abnormal elevation of creatinine within the blood. Such as:
• ▪️glomerulonephritis
• ▪️pylonephritis
• ▪️acute tubular necrosis
• ▪️urinary obstruction

There are slight increases in creatinine levels after meals, especially after ingestion of large quantities of meat.

Serum creatinine and Urea

The elderly normally have lower creatinine levels due to reduced muscle mass. This may potentially mask renal disease in patients of this age group.

• A diet high in meat content can cause transient elevations of serum creatinine.

• Drugs that may increase creatinine values include aminoglycosides (ie: getamicin), cimetidine, and other nephrotoxic drugs such as cephalosporins (ie: cefoxitin)

(Diseases affecting renal function) Which may include:

• Glomerulonephritis

• Pyelonephritis

• Acute tubular necrosis

• Urinary tract obstruction

• Reduced renal blood flow (ie: shock, dehydration, congestive heart failure, atherosclerosis)

• Diabetic nephropathy

• Nephritis

CT with contrast.

“Contrast Induced Nephropathy” order set

Adult: < 500 ug FEU/L

a substance released as a blood clot breaks up. Ddimer levels are often higher than normal in people who have a blood clot.

In current practice, the most common indication for this test would be to rule out Pulmonary Embolus 8 (PE) or Deep Vein Thrombosis (DVT) 9 .

The fragment D-dimer assesses both thrombin and plasmin activity. D-dimer is a fibrin degradation fragment that is made through fibrinolysis. As plasmin acts on the fibrin polymer clot, FDP’s and D-dimer are produced. D-dimer is a highly specific measurement of the amount of fibrin degradation that occurs. Normal plasma does not have detectable amounts of fragment D-dimer. Levels of D-dimer can also increase when a fibrin clot is lysed by thrombolytic therapy. Thrombotic problems such as deep-vein thrombosis, pulmonary embolism, can be part of the complex clinical assessment using the D-dimer levels.

• Disseminated intravascular coagulation (DIC):

This is a serious bleeding disorder resulting from abonormally initiated and accelerated clotting. The ensuing depletion of clotting factors and platelets may lead to uncontrollable hemorrhage.

DIC is always caused by an underlying disease (e.g. Multiple organ failure, mass transfusions). The underlying disease must be treated for the DIC to resolve.

• Primary fibrinolysis

• Deep-vein thrombosis

• Pulmonary embolism

• Vasoocclusive crisis of sickle cell anemia

• Surgery:

These clinical situations are associated with varying degrees of clotting and fibrinolysis. D-dimer is produced by the action of plasmin on the fibrin polymer clot.

• ▪️ Heart failure - 0.5-2.0 ng/ml
• ▪️ Arrhythmia - 1.5-2.0 ng/ml

takes approximately one to two weeks to reach a steady level in the blood and in the target organ, the heart.

• Dizziness

• Blurred vision or seeing yellow or green halos

• Vomiting

• Diarrhea

• Irregular heartbeat

• Difficulty breathing

• Fatigue

• Shortness of breath

• Swelling in the hands and feet (edema)

• Characteristic EKG changes include bradycardia 11 (the most frequent vital sign abnormality in toxicity), a prolonged PR interval

Digoxin is primarily cleared from your system by the kidneys. When someone has kidney problems, their doctor may want to monitor kidney function and blood potassium levels since kidney dysfunction and low levels of potassium can result in symptoms of digoxin toxicity.

Once the dosage level is determined, digoxin levels are monitored routinely, at a frequency determined by the doctor, to verify correct dosage and if any changes occur in drug source, dosage, or other medications taken at the same time.

Changes in health status can affect levels of digoxin and its ability to control symptoms. Digoxin tests may be done and the dose adjusted if necessary when someone experiences a physiologic change that may affect blood levels and effectiveness of digoxin. This may be when someone develops, for example, kidney or thyroid problems, cancer, or stomach or intestinal illness.

Adult: 90-120 ml/min

It is performed by ordering a creatinine test and calculating the eGFR. The creatinine test is ordered frequently as part of a routine Comprehensive Metabolic Panel (CMP) or Basic Metabolic Panel (BMP), or along with a Urea (or BUN) test whenever a doctor wants to evaluate the status of the kidneys. It is ordered to monitor those with known kidney disease and those with conditions such as diabetes and hypertension that may lead to kidney damage.

The GFR test is used to screen for and detect early kidney damage and to monitor kidney status. Glomerular filtration rate (GFR) is a calculation that determines how well the blood is filtered by the kidneys, which is one way to measure remaining kidney function. Glomerular filtration rate is usually calculated using a mathematical formula that compares a person's size, age, sex, and race to serum creatinine levels.

Kidney Function.

• Swelling or puffiness, particularly around the eyes or in the face, wrists, abdomen, thighs, or ankles

• Urine that is foamy, bloody, or coffee-colored

• A decrease in the amount of urine

• Problems urinating, such as a burning feeling or abnormal discharge during urination, or a change in the frequency of urination, especially at night

• Mid-back pain (flank), below the ribs, near where the kidneys are located

• High blood pressure (hypertension)

• Urinating more or less often

• Feeling itchy

• Tiredness, loss of concentration

• Loss of appetite, nausea and/or vomiting

• Swelling and/or numbness in hands and feet

• Darkened skin

• Muscle cramps

A person's GFR decreases with age and some illnesses. There is different equation that should be used to calculate the GFR for those under the age of 18.

A GFR test may not be as useful for those who differ from normal creatinine concentrations. This may include people who have significantly more muscle (such as a body builder) or less muscle (such as a muscle-wasting disease) than the norm, those who are extremely obese, malnourished, follow a strict vegetarian diet, ingest little protein, or who take creatine dietary supplements.

Important to note GFR equations are not valid for those who are 75 year of age or older because muscle mass normally decreases with age.

Determined when fasting

• Adult: 4.0 – 8.3 mmol/L Elderly:
• Increase in normal range after age 50 years

Through multiple feedback mechanisms, glucose levels are primarily controlled by insulin and glucagons, though many other things can affect the glucose level in the blood. Glucagon12 breaks glycogen down to glucose in the liver and glucose levels rise. Glucose levels are elevated after eating. Insulin, which is made in the beta cells of the pancreatic islets of Langerhans, is secreted. Insulin attaches to insulin receptors in muscle, liver and fatty cells in which it drives glucose into these target cells to be metabolized to glycogen, amino acids and fatty acids. Blood glucose levels diminish.

• Commonly used
• ▪️in evaluation of diabetic patients
• ▪️septic patients
• ▪️any patient with altered mental status

• Many forms of stress (ie: trauma, general anesthesia, infection, burns, MI, can cause increased serum glucose levels).

• Caffeine may cause increased levels.

• Most IV fluids contain dextrose, which is quickly converted to glucose. Most patients receiving IV fluids will have increased glucose levels.

• Drugs that may cause increased levels include antidepressants (tricyclics), betaadrenergic blocking agents, corticosteroids, IV dextrose infusion, diuretic, Epinephrine, estrogens, glucagons, lithium, phenothiazines, phenytoin, and salicylates (acute toxicity).

(Hyperglycemia)

• Diabetes mellitus (DM) This disease is defined by glucose intolerance.

• Acute stress response Severe stress, including infection, burns and surgery stimulates catecholamine release. This in turn stimulates glucagon secretion which causes hyperglycemia.

• Chronic renal failure Glucagon is metabolized by the kidney. With loss of kidney function, glucagon and glucose levels rise.

• Acute pancreatitis. As cells are injured during the inflammation process, the contents of the pancreatic cells (including glucagon) are spilled into the bloodstream. The glucagon causes hyperglycemia.

• Diuretic therapy Certain diuretics cause hyperglycemia.

• Corticosteroid therapy Cortisol causes hyperglycemia (response to stress and to sepsis).

(Hypoglycemia)

• Insulin overdose This is the most common cause of hypoglycemia. Insulin is administered at too high of a dose (especially in brittle diabetes) and glucose levels fall.

• Insulinoma Insulin is autonomously produced without regard to biofeedback mechanisms.

• Hypothyroidism Thyroid hormones affect glucose metabolism. With diminished levels of this hormone, glucose levels fall.

• Addison disease Cortisol affects glucose metabolism. With diminished levels of this hormone glucose levels fall.

• Extensive liver disease Most glucose metabolism occurs in the liver. With decreased liver function, glucose levels decrease.

• Starvation With decreased carbohydrate ingestion, glucose levels diminish.

The following symptoms may be associated with acute or chronic hyperglycemia, with the first three composing the classic hyperglycemic triad:

• Polyphagia - frequent hunger, especially pronounced hunger

• Polydipsia - frequent thirst, especially excessive thirst

• Polyuria - frequent urination

• Blurred vision

• Fatigue (sleepiness).

• Weight loss

• Poor wound healing (cuts, scrapes, etc.)

• Dry mouth

• Dry or itchy skin

• Tingling in feet or heels

• Erectile dysfunction

• Cardiac arrhythmia

• Stupor

• Coma

• hunger

• shakiness

• nervousness

• sweating

• dizziness or light-headedness

• sleepiness

• confusion

• difficulty speaking

• anxiety

• weakness

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