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.
