Blood chemistry lab values Flashcards
ACTH (adrenocorticotropic hormone)
AM: < 80 pg/mL (< 18 pmol./L)
PM: < 50 pg/mL (< 11 pmol/L
The serum ACTH study is a test of anterior pituitary gland function that affords the greatest insight into the causes of either Cushing syndrome (overproduction of cortisol) or Addison disease
(underproduction of cortisol).
Increased levels: Addison disease,
The reduced serum level of cortisol is a strong stimulus to pituitary production of ACTH), Stress: ACTH is overproduced as a result of neoplastic overproduction of ACTh in the pituitary or elsewhere in the body by and ACTH-producing cancer. Stress is a potent stimulus to ACTH production.
Decreased levels: Hypopituitarism: the pituitary gland is incapable of producing adequate ACTH.
Exogenous steroid administration: Overproduction or availability of cortisol is a strong inhibitor to
pituitary production of ACTH.
Anion gap
16 + 4 mEq/L (if potassium is used in the calculation)
12 +4 mEq/L (if potassium is not used in the calculation)
Calculation of the anion gap assists in the evaluation of patients with acid-base disorders. It is used to attempt to identify the potential cause of the disorder and can also be used to monitor therapy for acid-base abnormalities.
increased levels indicate: Lactic acidosis, diabetic acidosis, alcoholic ketoacidosis, alcohol intoxication, starvation (These diseases are associated with increased acid ions such as lactate, hydroxybutyrate, or acetoacetate. Bicarb neutralizes these acids, bicarb levels fall and AG mathematically increases.
Renal failure
Increased gastrointestinal losses of bicarbonate (ex. diarrhea or fistuale)
Hypoaldosteronism
Decreased levels: excess alkali ingestion( increase in alkali products (antiacids, boiled milk), especially in children, causes increased bicarb products and mathematically decrease AG. Multiple myeloma Chronic vomiting or gastric suction Hyperaldosteronism H (alypoproteinemia Lithium toxicity
ALT (alanine aminotransferase, formerly SGOT)
Elderly: may be slightly higher than adult values
Adult/child: 4-36 international units/L @ 37 C
Values may be higher in men and in African Americans
Infant: may be twice as high as adult values
This test is used to identify hepatocellular diseases of the liver. Its is also an accurate monitor of improvement or worsening of these diseases. In jaundiced patients an abnormal ALT will incriminate the liver rather than red blood cell hemolysis as a source of the jaundice. ALT is found predominately in the liver;lesser quantities are found in the kidneys, heart, and skeletal muscle. Injury or disease affecting the liver parenchyma will cause a release of this hepatocellular enzyme into the bloodstream, thus elevating serum ALT levels.
Significantly increased levels: Hepatitis, hepatic ischemia, hepatic necrosis,
moderately increased levels: cirrhosis, cholestasis, hepatic tumor, hepatotoxic drugs, obstructive jaundice, severe burns, trauma to striated muscle
mildly increased levels: myositis, pancreatitis, myocardial infarction, infectious mononucleosis, and shock.
Alkaline Phosphatase
Elderly: slightly higher than adults Adult: 30-120/L (0.5-2.0 microKat/L) Child/adolescent < 2 years: 85-235 2-8 years: 65-210 9-15 years: 60-300 16-21 years: 30-200
ALP is used to detect and monitor diseases of the liver or bone.
ALP is found in the liver and biliary epithelium. It is normally excreted into the bile. Obstruction, no matter how mild, will cause elevations in ALP.
Young children have increased ALP levels because their bones are growing. This increase is magnified during the “growth spurt,” which occurs at different ages in males and females.
Ammonia (plasma)
Adult 10-80 mcg/dL or 6-47 micromole/L
Child: 40-80 mcg/dL
Newborn: 90-150 mcg/dL
The liver normally converts ammonia, a byproduct of protein metabolism, into urea, which is excreted by the kidneys. When the liver is unable to convert ammonia to urea, toxic levels of ammonia accumulate in the bloodstream. Increased ammonia levels, which occur in liver dysfunction, may be due either to blood not circulating through the liver well or to actual hepatic failure. Ammonia is used to support the diagnosis of severe liver diseases (fulminant hepatitis or cirrhosis), and for surveillance of these diseases. Ammonia levels are also used in the diagnosis and follow-up of hepatic encephalopathy.
Amylase
60-120 units/dL 30-220 units/L
Amylase, an enzyme that helps with the digestion of starch, is found in high concentrations in the salivary glands and in the pancreas, each of which contains a different isoenzyme. These two isoenzymes can be separated to rule out nonpancreatic sources. Clients with bulimia nervosa often have enlarged salivary glands and elevated serum amylase levels. An amylase test may be used to see if induced vomiting is still occurring during treatment.
Pancreatitis is the most common reason for marked elevations in serum amylase, which begins to increase about 3 to 6 months after an attack to this disease. The severity of the the disease is not always direcetly related to the levels of the enzyme. In fact, about 10 % of patients with fatal pancreatitis have normal serum amylase levels. Renal failure may also cause abnormal elevations not related to pancreatic disease. Certain tumors, such as pheochromocytomas, myelomas, and bronchial cell carcinomas, are associated with high amylase levels.
AST (Aspartate aminotransferase formerly SGOT)
0-35 units/L (0-0.58 microKat/L)
can be used to detect liver necrosis.
AST is found predominately in heart, liver, and muscle tissue, although all tissues contain some of the enzyme. The highest amounts of them are found in high-energy cells such as the heart, liver and skeletal muscle.
Bicarbonate
23-30 mEg/L (23-30 mmol/L)
Bicarb functions as an important buffer in the bloodstream. To keep the pH in the bloodstream between 7.35-7.45. The loss of hydrogen, potassium, and chloride ions all contribute to the development of metabolic alkalosis. First, any loss of hydrogen ions causes a proportional increase in the bicarbonate side of the bicarb-carbonic acid buffering system. Secondly, when potassium is low in the serum, the kidneys are unable to excrete bicarb normally, Third, when chloride , a negative ion, is decreased in the bloodstream, another negative ion is needed to keep the positive and negative ions balanced in the serum. Thus, the kidneys cause the retention of bicarb to replace the missing chloride.
pg. 151-156 in corbett
Bilirubin
Total:
Unconjugated (Indirect, lipid soluble waste can pass through the blood brain barrier)
Conjugated (Direct, water-soluble)
0.3-1.0 mg/dL (5.1-17 micromole/L)
The total serum Bilirubin level is the sum of the conjugated (direct) and unconjugated (indirect) bilirubin.
0.2-0.8 mg/dL (3.4-12.0 micromole/L)
0.1-0.3 mg/dL (1.75-5.1 micromole/L)
An enzyme, glucuronyl transferase, is necessary for the transformation, or conjugation of bilirubin. Either a lack of glucuronyl transferase or the presence of drugs that interfere with this enzyme renders the liver unable to conjugate bilirubin. When bile reaches the intestine via the common bile duct, the bilirubin is acted on by bacteria to form chemical compounds called urobilinogens. Jaundice is recognized when the total serum bilirubin exceeds 2.5 mg/dL. Jaundice results from a defect in the normal metabolism or excretion of bilirubin. This defect can occur at any stage of heme catabolism. Once the jaundice is recognized either clinically or chemically, it is important (for therapy) to differentiate whether it is predominately caused by indirect or direct bilirubin. In general, jaundice caused by hepatocellular dysfunction (ex. hepatitis) results in elevated levels of INDIRECT bilirubin. This dysfunction usually cannot be repaired surgically. On the other hand, jaundice resulting from extrahepatic(posthepatic) dysfunction (gallstones obstructing the bile duct or a tumor doing that) results in elevated levels of DIRECT bilirubin; this type of jaundice usually can be resolved by open surgery or endoscopic surgery. Normally the indirect bilirubin makes up 70%-85% of the total bilirubin. In patients with jaundice, when more than 50% of the bilirubin is direct, it is considered a direct hyperbilirubinemia from gallstones, tumor, inflammation, scarring (cirrhosis) or obstruction of the extrahepatic ducts. Indirect hyperbilirubinemia is diagnosed when less than 15% to 20% of the total bilirubin is direct bilirubin. Diseases that typically cause this from of jaundice include accelerated erythrocyte hemolysis, hepatitis, or drugs. Physiologic jaundice of the newborn occurs if the newborn’s liver is immature and does not have enough conjugating enzymes. This results in a high circulating blood level of unconjugated bilirubin, which can pass through the blood brain barrier and deposti in the brain cells of the newborn, causing encephalopathy (kernicterus)
ANP(Atrial natriuretic Peptide)
BNP (Brain natriuretic peptide)
22-77 pg/mL (22-77 ng/L)
< 100 pg/mL (22-77 ng/L)
Natriuretic peptides are neuroendocrine peptides that oppose the activity of the renin-angiotensin system. ANP is synthesized in the cardiac atrial muscle. The main source of BNP is the cardiac ventricle. The cardiac peptides are continuously released by the heart muscles cells in low levels. BUT, the rate of release can be increased by a variety of neuroendocrine and physiologic factors, including hemodynamic load, to regulate cardiac preload and afterload. Because of these properties, BNP and ANP have been implicated in the pathophysiology of hypertension, CHF< and atherosclerosis. Both ANP and BNP are released in response to increased atrial and ventricular stretch or pressure (ex that would cause this are: CHF, MI, systemic hypertension, Heart transplant rejection, cor pulmonale {enlargement of the right ventricle of the heart as a response to increased resistance or high blood pressure in the lungs (pulmonary hypertension. aka right sided heart failure} respectively, and will cause vasorelaxation (dilation), inhibition of aldosterone secretion from the adrenal gland and renin from the kidney, thereby increasing natriuresis (excretion of sodium) and reduction in blood volume(diuresis). All of theses actions work in concert on the vessels, heart, and kidney to decrease the fluid load on the heart, allowing the heart to function better and improving cardiac performance. BNP, in particular, correlates well to left ventricular pressures. As a result, BNP is a good marker for CHF. BNP levels, by themselves, are more accurate than any historical or physical findings or laboratory values in identifying CHF as the cause of dyspnea. The higher the levels of BNP are, the more the severe the CHF. This test is used in urgent care setting to aid in the differential diagnosis of shortness of breath. If BNP is elevated, the SOB is because of CHF. If BNP levels are normal, the SOB is pulmonary and not cardiac.
Calcium
Total: 9.0-10.6 mg/dL (2.25-2.75 mmol/L)
Ionized: 4.5-5.6 mg/dL (1.05-1.30)
Critical values: < 6 or >13 mg/dL or 3.25 mmol/L
Ionized calcium: < 2.2 or > 7 mg/dL or 1.58 mmol/L
The serum calcium test is used to evaluate parathyroid function and calcium metabolism by directly measuring the total amount of calcium in the blood. Serum calcium levels are used to monitor patients with renal failure, renal transplantation, hyperparathyroidism, and various malignancies. They are also used to monitor calcium levels during and after large-volume blood transfusions.
About one half of the total calcium exists in the blood in its free (ionized) form, and about one half exits in its protein-bound form (mostly with albumin). The serum calcium level is a measure of both. As a result, when the serum albumin level is low (as in malnourished patients), the serum calcium level will also be low, and vice versa. As a rule of thumb, the total serum calcium level decreases by approximately 0.8 mg for every 1-g decrease in the serum albumin level. Serum albumin should be measure with serum calcium.
Calcitonin, a hormone secreted by the thyroid gland, protects against a calcium excess in the serum. PTH, secreted by the parathyroid gland, keeps a sufficient level of calcium in the bloodstream; an increase in PTH also decreases phosphorus levels.
Common causes of Hypercalcemia:
False rise caused by dehydration (dehydration causes the serum to be concentrated therefore rising serum levels because of fluid loss).
Hyperparathyroidism (serum phosphate level decreased)
Malignant tumors can cause elevated calcium levels in two main ways. FIrst, tumor metastasis (myeloma, lung, breast, renal cell) to the bone can destroy the bone, causing resorption and pushing calcium into the blood. Second, the cancer (lung, breast, renal cell) can produce a PTH-like substance that drives the serum calcium up (ectopic PTH).
Immobilization
Thiazide diuretics
Vitamin D intoxication (increase absorption of calcium in the GI tract and renal)
Common causes of hypocalcemia:
False decrease caused by low albumin levels
hypoparathyroidism (serum phosphate levels increased)
early neonatal hypocalcemia
chronic renal disease (serum phosphate level increased)
pancreatitis
massive blood transfusions
severe malnutrition
Carcinoembryonic antigen (CEA)
<5 ng/mL (5 mcg/L)
This tumor marker is used for determining the extent of disease and prognosis in patients with cancer (especially gastrointestinal or breast). It is also used in monitoring the disease and its treatment.
CEA is a protein that normally occurs in fetal gut tissue. By birth, detectable serum levels disappear.
It was originally thought to be a specific indicator of the presence of colorectal cancer. Subsequently, however, this tumor marker has been found in patients who have a variety of carcinomas (breast, pancreatic, gastric, hepatobiliary), sarcomas, and even many benign diseases ( ulcerative colitis, diverticulitis, cirrhosis). Chronic smokers also have elevated CEA levels.
Because the CEA level can be elevated in both benign and malignant diseases, it is not a specific test for colorectal cancer. Furthermore, not all colorectal cancers produce CEA. Therefore CDEA is not a reliable screening test for the detection of colorectal cancer in the general population.
This test is also used in the surveillance of patients with cancer. A steadily rising CEA level is occasionally the first sign of tumor recurrence. This makes CEA testing very valuable in the follow-up of patients who have already had potentially curative therapy. CEA can also be detected in body fluids other than blood. Its presence in those body fluids indicates metastasis. This test is commonly performed on peritoneal fluid or chest effusions. Elevated CEA levels in these fluids indicate metastasis to the peritoneum or pleura, respectively. Likewise, elevated CEA levels in the cerebrospinal fluid indicate central nervous system metastasis.
Chloride
98-106 mEq/L (98-106 mmol/L)
Critical value: 115 mEq/L
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. Its primary purpose is to maintain electrical neutrality, mostly as a salt with sodium. It follows sodium (cation) losses and accompanies sodium excesses in an attempt to maintain electrical neutrality. for example, when aldosterone encourage sodium reabsorption, chloride follows to maintain electrical neutrality.
Hypochloremia and hyperchloremia rarely occur alone and usually are part of parallel shifts in sodium or bicarb levels. Signs and symptoms of hypochloremia include hyperexcitability of the nervous system and muscles, shallow breathing, hypotension, and tetany. Signs and symptoms of hyperchloremia include lethargy weakness, and deep breathing.
Cholesterol
Adult/elderly or = to 240 mg/dL
Cholesterol is the main lipid associated with atertiosclerotic vascular disease. Cholesterol, however, is require for the production of steroids, sex hormones, bile acids, and cellular membranes. Most of the cholesterol we eat comes from foods of animal origin. The liver metabolizes the cholesterol to its free form, and cholesterol is transported in the bloodstream by lipoproteins. Nearly 75% of the cholesterol is bound to low-density lipoproteins(LDL), and 25% is bound to high-density lipoproteins(HDL). Cholesterol is the main component of LDL and only a minimal component of HDL and very-low-density lipoprotein (VLDL). It is the LDL that is most directly associated with increased risk for CHD.
Cortisol
Time -0800: 5-23 mcg/dL (138-635 nmol/L)
1400: 3-13 mcg/dL (83-359 nmol/L)
This test is performed on patients who are suspected to have hyperfunctioning or hypofunctioning adrenal glands.
Increased serum cortisol level: An increase in cortisol can be either ACTH-dependent or ACTH-independent. A pituitary tumor can cause an increase of ACTH, which causes and increased cortisol level. This type of cortisol increase is ACTH-dependent, and it is sometimes called Cushing’s DISEASE. Increases of serum cortisol from other causes are called Cushing’s SYNDROME.
Plasma cortisol levels increase independently of the pituitary gland when there is hyperplasia of the adrenal cortex. Hypersecreting tumors of the adrenal cortex may be malignant or benign.
Some nonendocrine malignant tumors can secrete ACTH, which can result in increased serum cortisol levels. Cushing’s syndrome can be caused by the administration of corticosteroids over a long period of time.
Creatinine
Adult male: 0.6-1.2 mg/dL (53-106 micromole/L)
Adult female: 0.5-1.1 mg/dL (44-97 micromole/L)
Critical value: >4 mg/dL (indicates serious impairment in renal function)
Creatinine is a catabolic product (waste 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 blood urea nitrogen (BUN), is excreted entirely by the kidneys and therefore is directly proportional to renal excretory function, so it is used to diagnose impaired renal function.Thus, with normal excretory function, the serum creatinine level should remain constant and normal. Besides dehydration, only renal disorders, such as glomerulonephritis, pyelonephritis, acute tubular necrosis, and urinary obstruction, will cause an abnormal elevation in creatinine. There are slight increases in creatinine levels after meals, especially after ingestion of large quantities of meat. furthermore, there may be some diurnal variation in creatinine (nadir at 7am and peak at 7pm). Unlike BUN, the creatinine level is affected minimally by hepatic function. The serum creatinine level has much the same significance as the BUN level but tends to rise later. Therefore elevations in creatinine suggest chronicity of the glomerular filtration rate. The creatinine level is interpreted in conjunction with the BUN. These tests are referred to as renal function studies:The BUN/ creatinine ratio is a good measurement of kidney and liver function. The normal range is 6 to 25, with 15.5 being the optimal adult value for this ratio.
Ferritin
Male: 12-300 mcg/mL
Female: 10-150 mcg/mL
A ferritin level of below 10 mg/100/mL is diagnostic of iron deficiency anemia
Ferritin, the predominant iron storage, is directly related to the amount of storage in a healthy adult. This is the most sensitive test to determine iron-deficiency anemia. In normal patients, 1 ng/mL of serum ferritin corresponds to approximately 8 mg of stored iron. Ferritin levels rise persistently in males and postmenopausal females. In premenopausal females, levels stay about the same. Decreases in ferritin levels indicate a decrease in iron storage associated with iron-deficiency anemia. A decrease in serum ferritin level often precedes other signs of iron deficiency, such as decreased iron levels or changes in red blood cell size, color, and number. Only when protein depletion is severe can ferritin be decreased by malnutrition. Increased levels are the sign of iron excess, as seen in hemochromatosis, hemosiderosis, iron poisoning, or recent blood transfusions. Increases in ferritin are also noted in patients with megaloblastic anemia, hemolytic anemia, and chronic hepatitis. Illness such as infections, inflammations, and malignant diseases causes increased levels and thus may make ferritin level unreliable as an indicator of iron stores.
Illness such as infections, inflammations, and malignant diseases cause increased levels and thus may make ferritin level unreliable as an indicator of iron stores. If there are no chronic illnesses, serum ferritin determination is reliable test for detecting iron deficiency.
GGT (Gamma-Glutamyl Transferase)
< 45 years of age (female): 5-27 units units/L
> 45 years of age (male and female): 8-38 units/L
THis is an enzyme that is useful in amino acid transport across the cell membrane.It’s cheifly in the liver, kidney, prostate and spleen. When ALP is elevated, the GGT may be used to assess whether the increase is due to liver and biliary involvement, because the GGT is more specific for the hepatobiliary system, whereas the ALP can be elevated in bone or liver disease. This test is highly accurate in indicating even the slightest degree of cholestasis. THis is the most sensitive liver enzyme for detecting biliary obstruction, cholangitis, or cholecystitis. The GGT is also raised by raised by alcohol and hepatotoxic drugs and thus is useful to monitor drug toxicity and alcohol abuse.
HgbA1C (Glycosolated hemoglobin)
Non-diabetic adult: 2.2%-4.8%
Good diabetic control: 2.5%-5.9%
Fair diabetic control: 6%-8%
Poor diabetic control: > 8%
In adults about 98% of the hemoglobin in the RBC is hemoglobin A. About 7% of hemoglobin A consists of a type of hemoglobin (HbA1) that can combine strongly with glucose in a process called glycosylation. Once Glycosylation occurs, it is not easily reversible. HbA1 is actually made up of three components (hemoglobin A1a, A1b, A1c,). HbA1c is the component that mostly strongly combines glucose. HbA1c makes up the majority of the HbA1. About 70% of HbA1c is glycosylated. ONly 20% of A1a and A1b are glycosylated. HbA1c is the most accurate measurement, because this is the majority of glycosylated hemoglobin.
As the RBC circulates, it combines its HbA1 with some of the glucose in the bloodstream to form glycohemoglobin (GHb). The amount of GHb depends on the amount of glucose available in the bloodstream over the RBC’s 120-day life span. Therefore determination of the GHb value reflects the average blood sugar level for the 100-to 120 day period before the test. The more glucose the RBC is exposed to, the greater the GHb percentage. One important advantage of this test is that the sample can be drawn at any time, because it is not affected by short-term variations (ex. food intake, exercise, stress, hypoglycemic agents, patient cooperation). It is also possible for very high short-term blood glucose to cause an elevation of GHb. Usually, however, the degree of glucose elevation results not form a transient high level but from persistent, moderate elevation over the entire life of the RBC>
Homocysteine
4-14 micromole/L
This is an important predictor of coronary, cerebral, and peripheral vascular disease. When a strong familial predisposition or early-onset vascular disease is noted, homocysteine testing should be performed to determine if genetic or acquired homocysteine excess exists. Because elevated homocysteine levels are associated with vitamin B12 or folate deficiency, this is a reasonable test to use for the detection and surveillance of malnutrition. Homocysteine is an intermediate amino acid formed during the metabolism of methionine. Homocysteine appears to promote the progression of atherosclerosis by causing endothelial damage, LDL deposition (plaque formation), and promoting vascular smooth muscle growth causing vascular constriction and further diminishing the vessel lumen, thereby compounding the vascular occlusive results. Ischemic events in the cerebral, coronary, and peripheral tissues occur earlier, more severely, and more frequently. Screening for hyperhomocysteinemia (levels >15 micromole/L) should be considered in individuals with progressive and unexplained atherosclerosis despite normal lipoproteins and in the absence of other risk factors. It is also recommended in patients with an unusual family history of atherosclerosis, especially at a young age. a person with an elevated homocysteine level is also at a five-times increased risk for stroke, dementia, and Alzheimer disease. Elevated levels also appear to be a risk factor for osteoporotic fractures in older men and women.
Dietary deficiency of vitamins B6 and B12, or folate is the most common nongenetic cause of elevated homocysteine. These vitamins are essential cofactors involved in the metabolism of homocysteine to methionine. Because of the relationship of homocysteine to these vitamins, homocysteine blood levels are helpful in the diagnosis of deficiency syndromes associated with these vitamins. In patients with megaloblastic anemia, homocysteine levels may be elevated before results of the more traditional tests become abnormal. Therefore using homocysteine as an indicator may result in earlier treatment and thus improvement of symptoms in patients with these vitamin deficiencies. Some practitioners recommend homocysteine testing in patients with known poor nutritional status (alcoholics, drug abusers) and the elderly.
Insulin Assay
6-26 microunit/mL (43-186 pmol/L)
Newborn- 3-20 microunit/mL
Critical value >30 microunit/mL
This test is used to diagnose insulinoma (tumor of the islets of Langerhans) and to evaluate abnormal lipid and carbohydrate metabolism. It is used in the evaluation of patients with fasting hypoglycemia.
Increased levels may also indicate:
Cushing syndrome: the elevated glucose caused by the cortisol overproduction in patients with this syndrome acts as a constant stimulant to insulin.
Acromegaly : the elevated glucose level caused by growth hormone overproduction in the patient with acromegaly acts as a constant stimulant to insulin.
fructose or galactose intolerance: These complex sugars cannot be metabolized normally and, like glucose, stimulate insulin production.
Decreased levels: Diabetes: insulin dependent.
Hypopituitarism: This disease is associated with reduced thyroid and adrenal function along with reduced growth hormone levels. This leads to reduced glucose levels. Insulin production is diminished.
Iron
Male: 80-180 mcg/dL (14-32 micromole/L)
Female: 60-160 mcg/dL (11-29 micromole/L)
Abnormal levels of iron are characteristic of many diseases, including iron-deficiency anemia and hemochromatosis. As much as 70% of the iron in the body is found in the hemoglobin of the red blood cells. The other 30% is stored in the form of ferritin and hemosiderin. Iron is supplied by the diet. About 10% of the ingested iron is absorbed in the small intestine and transported to the plasma. There the iron is bound to a globulin protein called transferrin and carried to the bone marrow for incorporation into hemoglobin. The serum iron determination is a measurement of the quantity of iron bound to transferrin. Iron-deficiency anemia has many causes, including insufficient iron intake, inadequate gut absorption, increased requirements (as in growing children and late pregnancy), and loss of blood (as in menstruation, bleeding peptic ulcer, colon neoplasm). Iron deficiency results in a decreased production of hemoglobin, which in turn results in a small, pale (microcytic, hypochromic) RBC. A decrease in MCV and MCHC is also seen. A decreased serum iron level, elevated TIBC, and low transferrin saturation value are characteristic of iron-deficiency anemia. Iron overload or poisoning is called hemochromatosis or hemosiderosis. Excess iron is usually deposited in the brain, liver, and heart and causes severe dysfunction of theses organs. Massive blood cause elevated iron levels but only transiently. transfusions should be avoided before serum iron level determinations. Because serum iron levels may vary significantly during the day, the blood specimen should be drawn in the morning, especially when the results are used to monitor iron replacement therapy and should refrain from eating for approximately 12 hours to avoid artificially high iron measurements caused by eating food with a high iron content.
Increased levels serum iron levels:
Hemosiderosis (Hemosiderosis, or iron overload, is a pathological condition characterized by deposition of excess iron within the body tissues that normally do not containing iron. Hemosiderosis is usually secondary to a primary cause such as multiple blood transfusion, chronic hemodialysis, or hemolytic anemia (e.g., thalassemia). or hemochromatosis.
Decreased serum iron levels:
Insufficient dietary iron
chronic blood loss(irregular menses, uterine cancer, GI cancer, inflammatory bowel disease, diverticulosis, urologic tract (hematuria) cancer, hemangioma, arteriovenous malformation)
Inadequate intestinal absorption of iron (malabsorption, short-bowel syndrome)
pregnancy (late)
Total Iron-binding capacity (TIBC)
250-460 mcg/mL (45-82 micromole/L)
TIBC is a measurement of all proteins available for binding mobile iron. Transferrin represents the largest quantity of iron-binding proteins. Therefore TIBC is an indirect yet accurate measurement of transferrin. Ferritin is not included in TIBC, because it binds only stored iron. During iron overload, transferrin levels stay about the same or decrease, whereas the other less common iron-carrying proteins increase in number. In this situatino, TIBC is less reflective of true transferrin levels. TIBC is increased in 70% of patients with iron deficiency.
TIBC is more a reflection of liver function (transferrin is produced by the liver) and nutrition than of iron metabolism. TIBC values often are used to monitor the course of patients receiving hyperalimentation(the ingestion or administration of a greater than optimal amount of nutrients. Although the term hyperalimentation is commonly used to designate total or supplemental nutrition by intravenous feedings, it is not technically correct inasmuch as the procedure does not involve an abnormally increased or excessive amount of feeding).
Lactic Acid
Venous blood: 5-20 mg/dL (0.6-2.2 mmol/L)
Arterial blood: 3-7 mg/dL (0.3-0.8 mmol/L)
Measurement of lactic acid is helpful to document and quantify the degree of tissue hypoxemia associated with shock or localized vascular occlusion. It is also a measurement of the degree of success associated with treatment of those conditions.
Under conditions of normal oxygen availability to tissues, glucose is metabolized to CO2 and H2O for energy. When oxygen to the tissues is diminished, anaerobic metabolism of glucose occurs, and lactate (lactic acid) is formed instead of CO2 and H2O. To compound the problem of lactic acid buildup, when the liver is hypoxic, it fails to clear the lactic acid. Lactic acid accumulates, causing lactic acidosis. Therefore blood lactate is a fairly sensitive and reliable indicator of tissue hypoxia. The hypoxia may be caused by local tissue hypoxia (ex. mesenteric ischemia, extremity ischemia) or generalized tissue hypoxia such as exits in shock. Type 1 LA is caused by diseases that increase lactate but are not hypoxia related, such as glycogen storage diseases or liver diseases, or by drugs. LA caused by hypoxia is classified as type 2. Shock, convulsions, and extremity ischemia are the most common causes of type 2 LA. Type 3 LA is idiopathic and is most commonly seen in nonketotic patients with diabetes
Carbon monoxide poisoning can increase lactic acid levels too. It binds to hemoglobin more tightly than oxygen, therefore, no oxygen is available to the tissues for normal aerobic metabolism. Anaerobic metabolism occurs and lactic acid is formed, resulting in increased blood levels.
Magnesium
adult:1.3-2.1 mEq/L (0.65-1.05 mmol/L)
child: 1.4-1.7 mEq/L
newborn: 1.4-2 mEq/L
Critical: 3 mEq/L
Most of the magnesium is found in the body intracellularly. About half is in the bone. This electrolyte is critical in nearly all metabolic processes caused it is bound to an ATP molecule. carbohydrate, protein, and nucleic acid synthesis and metabolism depend on magnesium. Most organ functions, including neuromuscular tissue, also depend on magnesium. It is important to monitor magnesium levels in cardiac patients. Low magnesium levels may increase cardiac irritability and aggravate cardiac arrhythmias. Hypermagnesemia retards neuromuscular conduction and is demonstrated as cardiac conduction slowing (widen PR and Q-T intervals with wide QRS), diminished deep-tendon reflexes, and respiratory depression. Magnesium is closely related to calcium in that it increases the intestinal absorption of calcium. Magnesium is also important in calcium metabolism. Often hypocalcemia will respond to magnesium replacement.
Increased levels: renal insufficiency: magnesium is excreted by the kidneys. WIth end-stage renal failure, excretion is reduced and magnesium accumulates in the blood.
Addison disease: Aldosterone enhances magnesium excretion. With reduced aldosterone, magnesium excretion is diminished.
Ingestion of magnesium-containing antacids or salts:
Symptoms of increased magnesium levels include lethargy, nausea and vomiting, and slurred speech.
Decreased levels:
malnutrition
Malabsorption:
Hypoparathyroidism: In this disease, calcium levels are reduced. Calcium enhances intestinal absorption of magnesium, and with low calcium levels, magnesium is not well absorbed, so blood levels diminish. In hyperparathyroidism, calcium levels are high and magnesium levels increase.
Alcoholism: ethanol increases magnesium loss in urine
Chronic renal tubular disease: Magnesium is reabsorbed in the renal tubule. diseases affecting the area of the kidney (ex. tubular necrosis) or drugs that are toxic to the renal tubule (ex. aminoglycosides) will allow increased losses of magnesium in the urine.
Diabetic acidosis- with treatment of this disease, magnesium levels fall. As insulin is given to these patients to drive glucose into the cells, magnesium follows and blood levels drop.
Osmolality (serum)
Adult: 285-295 mOsm/kg H2O (285-295 mmol/kg)
critical values: 320 mOsm/kg H20.
This test is used to gain information about fluid status and electrolyte imbalance. It is also helpful in evaluating illnesses involving antidiuretic hormone (ADH). it measures the concentration of dissolved particles in the blood. Osmolality increases with dehydration and decreases with overhydration. There is an elaborate feedback mechanism that controls osmolality. Increased osmolality will stimulate secretion of ADH; this will result in increased water reabsorption in the kidney, more concentrated urine, and less concentrated serum. A low serum osmolality will suppress the release of ADH, resulting in decreased water reabsorption and large amounts of dilute urine. The simultaneous use of urine osmolality helps in the interpretation and evaluation of problems.
The test is very helpful in evaluating patients with seizures, ascites, hydration status, acid-base balance, and suspected ADH abnormalities. Osmolality is also helpful in identifying the presence of organic acids, sugars, or ethanol. In these cases there is and “Osmolal gap”. This gap represents the difference between what the osmolality should be based on calculations of serum sodium, glucose, and BUN (the three most important solutes in the blood) and the osmolality as truly measured. If the “gap” is large, solutes such as organic acids (ketones) or unusually high levels of glucose or ethanol by-products are suspected to present. Finally, Osmolality also plays an important role in toxicology and workups for coma patients. Values greater than 385 are associated with stupor in patients with hyperglycemia. When values of 400 to 420 are detected, grand mal seizures can occur. Values greater than 420 can be lethal.
Phosphorus, inorganic
Adults: 3.0-4.5 mg/dL (0.97-1.45 mmol/L)
elderly slightly lower than adults
Critical value: < 1mg/dL
Most of the phosphate in the body is part of organic compounds. only a small amount of total body phosphate is inorganic phosphate. It is the inorganic phosphate that is measured when a “phosphate”, “phosphorus”, “inorganic phosphorus”, or “inorganic phosphate” is requested. Most of the body’s inorganic phosphorus is intracellular and is combined with calcium within the skeleton; however, approximately 15% of the phosphorus exists in the blood as a phosphate salt. The organic phosphate (not measured in this test) is used to synthesize part of the phospholipid compounds in the cell membrane, ATP for energy source in metabolism, nucleic acids, or enzymes. The inorganic phosphate (measured in this test) contributes to electrical and acid-base homeostasis. Phosphate levels vary significantly during the day, with lowest values occurring around 10AM and highest values occurring 12 hours later. Dietary phosphorus is absorbed in the small bowel. The absorption is very efficient, and only rarely is phosphatemia caused by GI malabsorption.
Increased levels (hyperphosphatemia):
Hypoparathyroidism: renal reabsorption is enhanced(PTH tends to decrease phosphate reabsorption in the kidneys).
Renal failure
Increased dietary or IV intake of phosphorus:
acromegaly: renal reabsorption is enhanced.
Bone metastasis: The phosphate stores in the bones are mobilized by the destructive bone tumors.
Sarcoidosis: Intestinal absorption of phosphates is increased because of the vitamin D effect produced by granulomatous infections.
Hypocalcemia: Calcium and phosphates exist in an inverse relationship. When one is elevated, the other is low.
Acidosis: When the pH is reduced, phosphates are driven out of the cell and into the bloodstream as part of a buffering system.
Rhabdomyolysis
advanced lymphoma or myeloma
Hemolytic anemia: Cell lysis associated with the above disease causes intracellular phosphate to pour out into the bloodstream. Phosphate levels rise.
Decreased levels (hypophosphatemia)
chronic antacid ingestion: antacids bind the phosphate in the intestine and preclude absorption.
Hyperparathyroidism: PTH increases urinary excretion of phosphates.
Hypercalcemia
Chronic alcoholism
Vitamin D deficiency (rickets): renal tubules fail to reabsorb phosphates.
Hyperinsulinism: insulin tends to drive phosphates into the cells.
Malnutrition:
Alkalosis: Phosphate acts as a buffer. When pH increases, phosphate levels in the blood diminish because of an intracellular shift
Potassium (serum)
Adult: 3.5-5.0 mEq/L
Critical values: Adult 6.5 mEq/L
The intracellular potassium concentration is approximately 150 mEq/L, whereas the normal serum concentration is approximately 4 mEq/L. This ratio is the most important determinant in maintaining membrane electrical potential, especially in neuromuscular tissue. Because the serum potassium concentration is so small, minor changes in concentration have significant consequences. Potassium is excreted by the kidneys. There is no reabsorption of potassium form the kidneys. Therefore, if potassium is not adequately supplied in the diet (or by IV administration in the patient who is unable to eat), serum potassium levels can drop rapidly. It contributes to the metabolic portion of acid-base balance in that the kidneys can shift potassium for hydrogen ions to maintain a physiologic pH.
Serum potassium concentration depends on many factors, including:
1. Aldosterone( and, to a lesser extent, glucocorticosteroids). This hormone tends to increase renal losses of potassium.
2. Sodium reabsorption. As sodium is reabsorbed, potassium is lost.
3. Acid-base balance: Alkalotic state tend to lower serum potassium levels by causing a shift of potassium into the cell. Acidotic states tend to raise serum potassium levels by reversing that shift.
Symptoms of hyperkalemia include irritability, nausea, vomiting, intestinal colic, and diarrhea. The ECG may demonstrate peaked T waves, a widened QRS complex, and a depressed ST segment. Signs of hypokalemia are related to a decrease in contractility of smooth, skeletal, and cardiac muscles, which results in weakness, paralysis, hyporeflexia, ileus, increased cardiac sensitivity to digoxin, cardiac arrhythmias, flattened T waves, and prominent U waves. This electrolyte has profound effects on the heart rate and contractility. The potassium level should be followed in patients with Uremia, Addison disease, and vomiting and diarrhea and in patients taking steroid therapy and potassium-depleting diuretics. Potassium must be closely monitored in patients taking digitalis-like drugs, because cardiac arrhythmias may be induced by hypokalemia and digoxin.
a crush injury to tissues, hemolysis, infection will cause potassium within the cell is released into the bloodstream increasing serum levels.
Potassium in infused at slow rate to prevent irritation to the veins.
Prealbumin
15-36 mg/dL (150-360 mg/L)
Critical value: s short half-life, it is a sensitive indicator of any change affecting protein synthesis and catabolism. Therefore prealbumin is frequently ordered to monitor the effectiveness of total parenteral nutrition (TPN).
Prealbumin is significantly reduced in hepatobiliary disease because of impaired synthesis. Serum levels of prealbumin are better indicators of liver function than albumin levels. prealbumin is also a negative acute-phase reactant protein; which means serum levels decrease in inflammation, malignancy, and protein-wasting diseases of the intestines and kidneys. Because zinc is required for synthesis of prealbumin, low levels occur with zine deficiency. Increased levels of prealbumin occur in Hodgkin disease and chronic kidney disease.
Because of the low quantity of prealbumin in the serum, this protein is not often visualized on serum protein electrophoresis. However, because prealbumin crosses the blood-brain barrier, it is found in the CSF and can be seen on CSF electrophoresis(lumbar puncture).
Proteins
Total: 6.4-8.3 g/dL (64-83 g/dL)
Albumin: 3.5-5 g/dL (35-50 g/dL)
Globulin: 2.3-3.4 g/dL
Total serum protein is a combination of prealbumin, albumin, and globulins.
Albumin is a protein that is formed within the liver. It makes up approximately 60% of the total protein. The major effect of albumin within the blood is to maintain colloidal osmotic pressure. Furthermore, albumin transports important blood constituents such as drugs, hormones, and enzymes. Albumin is synthesized within the liver and is therefore a measure of hepatic function. When disease affects the liver cell, the hepatocyte loses its ability to synthesize albumin. The serum albumin level is greatly decreased. Because the half-life of albumin is 12 to 18 days, however, severe impairment of hepatic albumin synthesis may not be recognized until after that period.
Globulins are the key building block of antibodies. Their role in maintaining osmotic pressure is far less than that of albumin. These 2 are measures of nutrition. Malnourished patients, especially after surgery, have a greatly decreased level of serum proteins. Burn patients and patients who have protein-losing enteropathies and uropathies have low levels of protein despite normal synthesis. Pregnancy, Especially in the third trimester, is usually associated with reduced total proteins. In some diseases, albumin is selectively diminished, and globulins are normal or increased to maintain a normal protein level. For example, in collagen vascular diseases (ex. lupus erythematosus), capillary permeability is increased. Albumin, a molecule much smaller than globulin, is selectively lost into the extravascular space. Another group of diseases similarly associated with low albumin, high globulin, and normal total protein levels is chronic liver diseases. In these diseases the liver cannot produce albumin, but globulin is adequately made in the reticuloendothelial system. In both these types of diseases, the albumin level is low, but the total protein level is normal because of increased globulin levels. It is important to note that the albumin fraction of the total protein can be factitiously elevated in dehydrated patients.
Renin Assay (plasma) upright position, sodium depleted
Ages 20-39
>40 years
- 9-24 ng/mL/hr
- 9-10.8 ng/mL/hr
Renin is an enzyme released by the juxtaglomerular apparatus of the kidney into the renal veins in response to hyperkalemia, sodium depletion, decreased renal blood perfusion, or hypovolemia. Renin levels are affected by body position. Levels are higher in the upright position and decreased in the recumbent position. A high sodium diet causes a decrease in renin. Renin levels are increased with reduced salt intake, because reduced sodium levels are a stimulus to renin production. Thus, diet and the position of the client must be taken into account when using reference values for renin activity. Because the values of renin are normally higher in the morning, the test is performed early in the day. The client is usually in the supine position when the blood is drawn, but blood also may be drawn with the patient upright for comparison. Renin is no actually measured in this test. The plasma renin assay test actually measures, by radioimmunoassay, the rate of angiotensin 1 generation per unit time. This is a commonly used renin assay.
Renin Assay (plasma) Upright position, Sodium replaced
Ages 20-39
>40 years
- 1-4.3 ng/mL/hr
0. 1-3.0 ng/mL/hr
Sodium
136-145 mEq/L
The sodium content in the blood is a result of a balance between dietary sodium intake and renal excretion. Nonrenal (sweat) sodium losses normally are minimal. The serum level of sodium is not totally dependent on diet because the kidneys can conserve sodium when necessary. The hormone aldosterone causes a conservation of sodium and chloride and an excretion of more potassium. Natriuretic hormone, or third factor, is stimulated by increased sodium levels. This hormone decreases renal absorption and increases renal losses of sodium. Antidiuretic hormone, which controls the reabsorption of water at the distal tubules of the kidney, affects sodium serum levels by dilution or concentration. As free body water is increased, serum sodium is diluted and the concentration may decrease. The kidney compensates by conserving sodium and excreting water. If free body water were to decrease, the serum sodium concentration would rise; the kidney would then respond by conserving free water. Aldosterone, ADH (vasopressin), and natriuretic factor all assist in these compensatory actions of the kidney to maintain appropriate levels of free water. Symptoms of hyponatremia may begin when sodium levels are below 125 mEq/L. The first symptom is weakness. When sodium levels fall below 115 mEq/L, confusion and lethargy occur and may progress to stupor and coma if levels continue to decline. Symptoms of hypernatremia include dry mucous membranes, thirst, agitation, restlessness, hyperreflexia, mania, and convulsions.
Thyroid stimulating hormone (aka thyrotropin)
2-10 micro units/mL
The production of T4 (thyroxine) and T3 (triiodothyronine) is controlled by TSH from the anterior pituitary gland. TSH is released from the pituitary in response to the thyrotropin-releasing hormone (TRH) in the hypothalamus. Thus, like most of the other anterior pituitary hormones, TSH is sensitive to nervous response from the hypothalamus. Low levels of T3 and T4 are the underlying stimuli for TRH and TSH. Therefore A compensatory elevation of TRH and TSH occurs in patients with primary hypothyroid states, such as surgical or radioactive thyroid ablation; in patients with burned-out thyroiditis, thyroid agenesis, idiopathic hypothyroidism, or congenital cretinism; or in patients taking antithyroid medications. Measurement of TSH is useful in determining whether hypothyroidism is due to primary hypothyroidism, secondary hypofunction of the anterior pituitary gland, and Tertiary (hypothalamus) Hypothyroidism. In secondary or tertiary hypothyroidism the function of the pituitary or hypothalamus gland, respectively, is faulty as a result of tumor, trauma, or infarction. Therefore TRH and TSH cannot be secreted, and plasma levels of these hormones are near zero despite the stimulation that occurs with low T3 and low T4 levels. The TSH is used to monitor exogenous thyroid replacement or suppression as well. The goal of thyroid replacement therapy is to provide an adequate amount of thyroid medication so that TSH secretion is in the “ low normal range”, indicating a euthyroid state. The goal of thyroid suppression is to completely suppress the thyroid gland and TSH secretion by providing excessive thyroid medication. This treatment is used to diminish the size of a thyroid goiter. The dose of medication is given to keep the the TSH level less than 2 for replacement. Even lower TSH levels are preferred if thyroid suppression is the clinical goal. TSh and T4 levels are frequently measured to differentiate pituitary and thyroid dysfunction. A decreased T4 and normal or elevated TSH level can indicate a thyroid disorder. A decreased T4 with decreased TSH level can indicate a pituitary disorder. High doses of corticosteroids and dopamine infusions can suppress TSH levels.
Thyroxine, (T4)
Male: 4-12 mcg/dL
Female 5-12 mcg/dL
Adult >60: 5-11 mcg/dL
Triglycerides
Male: 40-160 mg/dL (0.45-1.81 mmol/L)
Female: 35-135 mg/dL (0.40-1.52 mmol/L)
These are neutral fat and oils that come from both animal fat and vegetable oils. A heavy meal or alcohol causes a transient increase in serum triglyceride levels, therefore, this test can indirectly be used to alcohol use. excess triglycerides, which are useful for energy, are stored in the body as adipose tissue. They are transported by very low density lipoproteins (VLDLs) and Low density lipoprotein(LDLs). Triglycerides are produced in the liver using glycerol and other fatty acids as building blocks. TGs constitute most of the fat in the body and are a part of a lipid profile that also evaluates cholesterol and lipoprotein. A lipid profile is performed to assess the risk of coronary and vascular disease.
Triiodothyronine uptake (T3 uptake)
24%-34% (24-34 arbitrary units- AU)
Blood Urea Nitrogen (BUN)
10-20 mg/dL (3.6-7.1 mmol/L) Elderly may be slightly higher than adults.
The BUN 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 catabolized and free ammonia is formed. The ammonia molecules are combined to form urea, which is deposited in the blood and transported to the kidneys for excretion. Therefore the BUN 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. Patients who have elevated BUN levels are said to have azotemia or be azotemic (azot, “nitrogen” + -emia, “blood condition”) is a medical condition characterized by abnormally high levels of nitrogen-containing compounds (such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds) in the blood. It is largely related to insufficient filtering of blood by the kidneys.[1] It can lead to uremia if not controlled. Azotemia has three classifications, depending on its causative origin, but all three types share a few common features. . Prerenal azotemia refers to elevation of the BUN as a result of pathologic conditions that affect urea nitrogen accumulation before it gets to the kidney. This is caused by a decrease in blood flow (hypoperfusion) to the kidneys. However, there is no inherent kidney disease. It can occur following hemorrhage, shock, volume depletion (dehydration), congestive heart failure, excessive protein catabolism, and narrowing of the renal artery among other things Another example of prerenal azotemia is gastrointestinal bleeding that causes variable and sometimes significant blood in the intestinal tract. The proteins in the blood and blood cells are digested to urea. As the marked increase in intestinal ura is absorbed, the BUN is expected to increase, sometimes significantly. If the disease is unilateral, however, the unaffected kidney can compensate for the diseased kidney and the BUN may not become elevated. Blockage of urine flow in an area below the kidneys results in postrenal azotemia. It can be caused by congenital abnormalities such as vesicoureteral reflux, blockage of the ureters by kidney stones, pregnancy, compression of the ureters by cancer, prostatic hyperplasia, or blockage of the urethra by kidney or bladder stones. Like in prerenal azotemia, there is no inherent renal disease. The increased resistance to urine flow can cause back up into the kidneys, leading to hydronephrosis. Finally, the synthesis of urea depends on the liver. Patients with severe primary liver disease will have a decreased BUN. With combined liver and renal disease ( as in hepatorenal syndrome), the BUN can be normal because poor hepatic functioning results in decreased formation of urea and is not an indicator that renal excretory function is adequate. The BUN is interpreted in conjunction with the creatinine test. These tests are referred to as “renal function studies.” The BUN/creatinine ratio is a good measurement of kidney and liver function. The normal adult range is 6 to 25, with 15.5 being the optimal value. The BUN:Cr in primary renal azotemia is less than 15. In cases of renal disease, glomerular filtration rate decreases, so nothing gets filtered as well as it normally would. However, in addition to not being normally filtered, what urea does get filtered is not reabsorbed by the proximal tubule as it normally would be. This results in higher levels of urea in the blood and lower levels of urea in the urine. Creatinine filtration decreases, leading to a higher amount of creatinine in the blood. Third spacing of fluids such as peritonitis, osmotic diuresis, or low aldosterone states such as Addisons Disease. The BUN:Cr in prerenal azotemia is greater than 20. The BUN:Cr in postrenal azotemia is initially >15. Over time the BUN:Cr will decrease due to tubule epithelial damage.[3] The increased nephron tubular pressure causes increased reabsorption of urea, elevating it abnormally relative to creatinine
.
Uric Acid
Male: 4.0-8.5 mg/dL (0.24-0.51 mmol/L)
Female: 2.7-7.3 mg/dL (0.16-0.43 mmol/L)
values in elderly may be slightly increased
Critical values: >12 g/dL
Uric acid is a nirogenous compound that is the final breakdown product of purine ( a DNA building block) catabolism. 75% of uric acid is excreted by the kidneys and 25% by the intestinal tract. When uric acid levels are elevated (hyperuricemia), the patient may have gout. Gout is a form of arthritis caused by deposition of uric acid crystals in periarticular tissue. Soft-tisse deposits of uric acid can also occur and are called tophi. Uric acid can become supersaturated in the urine and crystallize to form kidney stones that can block the ureters. Uric acid is made primarily in the liver. The blood level is determined by the rate of synthesis by the liver and the rate of excretion by the kidney. There is some variation of uric acid with age and sex. Causes of hyperuricemia can be overproduction or decreased excretion of uric acid (ex. kidney failure). Overproduction of uric acid may occur in patients with a catabolic enzyme deficiency that stimulates purine metabolism, or in patients with cancer, in whom purine and DNA turnover is great. Many causes of hyperuricemia are undefined and therefore labeled as idiopathic.
