Normal Range | ||
Males | Females | 1-3 years |
10 – 40 U/L | 9 - 25 U/L | 5 – 45 U/L |
Wednesday, October 13, 2010
(SGPT) Serum Glutamic Pyruvic Transaminase / Alkaline Aminotransferase (ALT)
serum Glutamic – Oxaloacetic Transaminase [SGOT] / Aspartate Aminotransferase [AST]
1. Aspartate Aminotransferase [AST]/ serum Glutamic – Oxaloacetic Transaminase [SGOT]
Introduction
Aminotransferases like ALT and AST that are concentrated in liver used as indicators of hepatocellular damage. Both parallel to each other but in alcohol related disease ALT is lower than AST.
Indications
Differential diagnosis of disease of hepatobiliary system and pancreas; repeat testing to establish chronicity of viral hepatitis; to check hepatotoxicity of a drug.
Normal levels | ||
Men | Women | 0-3 years |
10 – 40 U/L | 9 - 25 U/L | 20 – 60 U/L |
Increased in
Liver disease: Acute viral infections e.g. viral hepatitis A, B, C (value is increased up to 50 times the normal, peak levels up to 400 – 4000 U or more are reached during the icteric phase and gradually decline, during recovery phase); hepatotoxic drugs and chemicals (e.g. antifungals, narcotics and barbiturates, acetaminophen, salicylates); musculoskeletal disorders (myoglobinuria); acute myocardial infarction; acute pancreatitis; all common fevers (value raised up to 40 – 100 U) e.g. malaria, typhoid, extra pulmonary tuberculosis, dengue fever.Serum Globin
1. Serum Globin
Introduction
Globulins are produced by variety of tissue including liver. Serum globulins include alpha and beta globulins as well as serum immunoglobulins.
Normal range | |
Adults: 1.9 – 3.5 gm/Dl | Fetal: 0.4 – 3.7gm/dL |
Indications
To evaluate chronic liver diseases and cirrhosis (increases to varying degrees).
Increased in
Chronic liver diseases and cirrhosis; increase may be present in non- hepatic disorders or may reflect increased stimulation of peripheral reticuloendothelial compartment due to shunting of antigens past the liver and impaired clearance by kuffer cells.
Serum Albumin
1. Serum Albumin
Introduction
Albumin is quantitatively the most important serum protein synthesized by liver.
Indications
Marker of disorders of protein metabolism (e.g. nutritional, decreased synthesis increased loss).
Normal range
3.5 – 5.0 mg/dL
Increased in
Dehydration (relative increase); LV albumin infusion
Decreased in
Same as for total serum proteins.Total Serum Proteins
1. Total Serum Proteins
Introductions
Extensive liver injury may lead to decreased blood levels of albumin, prothrombin, fibrinogen and other proteins synthesized exclusively by hepatocytes. Serum protein levels are neither early nor sensitive indicators of liver disease.
Normal range
5.5- 8.5 mg/dL
Indications
Screening for nutritional deficiencies and gammopathies.
Increased in
Hypergammaglobulinemias, hypovolemic states.
Decreased in
Nutritional deficiency (e.g. malabsorption, Kwashiorkor, marasmus); decreased ineffective protein synthesis (e.g. severe liver disease, agammaglobulinemia increased loss (e.g. renal nephrotic syndrome); Gl disease (e.g. Protein losing enteropathies, surgical resection); severe skin disease (e.g. burns, eczema); plasmapheresis, increased catabolism (e.g. fever, inflammation, hyperthyroidism malignancy); dilutional (e.g. IV fluids administration, SIADH water intoxication).Saturday, August 21, 2010
Serum Bilirubin
Serum Bilirubin
Introduction
Spectrophotometric determinations of serum bilirubin in clinical laboratory measures two pigment fractions: (1) The water soluble conjugated fraction that gives a direct reaction with diazo reagent and consist largely of conjugated bilirubin. (2) The lipid soluble indirect – reaction fraction that represents primarily unconjugated bilirubin.
Indications
Differential diagnosis of disease of hepatobiliary system and pancreas and other
Causes of jaundice.
Normal levels | |
Total bilirubin | Direct bilirubin |
0.1 – 1.2 mg/dL | 0.03 – 0.5 mg/dL |
Increased in
Direct (conjugated) Bilirubin in
20 -40% of total: more suggestive of hepatic than posthepatic jaundice, 40 -60% of total: occur in either hepatic or posthepatic; > 50% of total: more suggestive of posthepatic than hepatic jaundice; total serum bilirubin > 40mg/dl indicates hepatocellular rather than extrahepatic obstruction.
Conditions
· Hereditary disorders (e.g. Dubin Johnson syndrome, Rotor's syndrome)
· Biliary duct obstruction (extra and intrahepatic)
· Hepatic cellular damage (viral, toxic, alcohol/ drug related)
· Infiltration, space – occupying lesions (e.g. metastatic tumor, abscess, granulomas)
Increased unconjugated (indirect) bilirubin in
Increased bilirubin production; hemolytic diseases (e.g. hemoglobinopathies, RBC enzyme deficiencies, disseminated intravascular coagulation (DIC), autoimmune hemolysis); ineffective erythropoiesis; blood transfusions; hematomas; hereditary disorders (e.g. Gilbert's disease, Crigler – Najjar syndrome); drugs causing hemolysis.Tuesday, August 17, 2010
Uric Acid
1. Uric Acid
Introduction
Uric acid levels are very labile and show day to day and seasonal variation in same person, also increased by emotional stress, total fasting, increased body weight, uric acid levels that do not correlate with the severity of kidney damage; urea and Creatinine are better.
Indications
Monitor chemotherapeutic treatment of neoplasms to avoid renal urate deposition with possible renal failure; monitor treatment of gout.
Normal Levels | ||
Males | Females | 1 –3 years |
4.0 – 8.6 mg/dL | 3 – 5.9 mg/dL | 1. 8 -5 |
Increased in
Renal failure; gout and also in 25% of relatives of patients of gout; asymptomatic hyperuricemia; leukemia, multiple myeloma, malignancies, lymphoma and other disseminated neoplasm and cancer chemotherapy; hemolytic and sickle cell anemia; toxemia of pregnancy; psoriasis (1/3 cases); drug use (barbiturates, methyl alcohol, salicylates, thiazides, furosemide, mitomycin, levodopa, phenytoin sodium); metabolic acidosis; diet (high protein, weight reduced diet).
Others von Gierke's disease, lead poisoning, Down's syndrome, polycystic kidney disease, atherosclerosis and hypertension (serum uric acid is increased in 80% of patients with elevated serum triglycerides).
Decreased in
Drugs (adrenocorticotropic hormone [ ACTH], high dose salicylates, probenecid, cortisone); Wilson's disease, Fanconi's syndrome, celiac disease, xanthuriaCreatinine
Creatinine
Introduction
Serum Creatinine is the most specific and sensitive indicator of renal disease. Use of BUN and Creatinine levels together is more informative in renal disorders.
Normal Range | |||
Male | Female | Fetal | Pregnancy |
0.7 - 1.4 mg/dL | 0.6 – 1.1 mg/dL | 0.4 – 0.9 mg/dL | 0.4 – 0.6 mg/dL |
Indications
Diagnosis of renal insufficiency
Increased in
Diet [ingestion of Creatinine (roast meat); prerenal azotemia; postrenal azotemia; impaired kidney function, 50% of renal function is needed to increase serum Creatinine from 1.0 – 2.0mg/dl. Therefore, not sensitive to mild – to moderate renal injury.
Decreased in
Pregnancy – normal value is 0.4 – 0.6 mg/dL. > 0.8mg/Dl is abnormal and should alert clinician to further diagnostic evaluation.
Blood Urea Nitrogen (BUN)
1. Blood Urea Nitrogen (BUN)
Introduction
BUN correlates with uremic symptoms better than serum creatinine.
Normal Range |
Adults: 7 –20mg/dL |
Neonate: 5 –18 mg/dL |
6 –8 mg/dL: associated with over hydration states |
50 – 150mg/dL: implies serious impairment of renal function |
150 –250mg/DL: is conclusive evidence of severely impaired glomerular function.
|
Indications
Differential diagnosis of various renal disorders; evidence of hemorrhage in Gl tract; assessment of patients requiring nutritional support in excess of catabolism (e.g. burns, cancer).
Increased in
Impaired kidney function; prerenal azotemia – ant case of reduced renal blood flow; congestive heart failure; salt and water depletion (vomiting, diarrhea, sweating); shock; postrenal azotemia – any obstruction of urinary tract (increased blood urea nitrogen [BUN] / Creatinine ratio); hemorrhage into Gl tract; AMI; stress.
Decreased in
Diuresis (e.g. with overhydration, often associated with low protein catabolism); severe liver damage (drug poisoning, hepatitis, other); increased utilization of protein for synthesis (late pregnancy, infancy, acromegaly, malnutrition ); diet (low protein and high carbohydrate, impaired absorption, malnutrition); nephritic syndrome; syndrome of inappropriate antidiuretic hormone secretion ( SIADH).Triglycerides (80% in VLDL 15% in LDL)
1. Triglycerides (80% in VLDL 15% in LDL)
Introduction
Triglyceride levels are not strong predictors of atherosclerosis or CAD and may not be an independent risk factor. Triglyceride levels are inversely related to HDL cholesterol levels.
Normal Range | |||
20 –170mg/dL | |||
Classification |
|
|
|
Normal Range | Borderline | High | Very high |
< 150mg/dL | 150 – 199mg/dL | 200 – 499mg/dL | > 500mg/dL |
Increased in
Genetic hyperlipidemias (e.g. Lipoprotein lipase deficiency, apo C..II deficiency, familial Triglyceridemia, dysbetalipoproteinemia); secondary hyperlipidemias (gout, pancreatitis, acute illness (e.g. in AMI rises to peak in 3 weeks and increase may persist for 1 year); drug use (e.g. thiazides, steroids, amiodarone, interferon).
Decreased in
Abetalipoproteinemia; malnutrition; vigorous exercise; drugs (e.g. ascorbic acid, clofibrate, phenformin, metformin, progestins).
LDL (Low Density Lipoprotein) cholesterol (Lipid Profile)
1. LDL (Low Density Lipoprotein) cholesterol
Introduction
LDL levels are directly related to risk fill CAD
Indication
Assess risk and decide treatment for CAD
Normal Levels
No coronary heart disease (CHD) and < 2 risk factors < 160mg/dL
No CHD but > 2 risk factors < 130mg/dL
Presence of CHD < 100mg/dL
Increased in
Familial hypercholesterolemia and combined hyperlipidemia; diabetes mellitus (DM) and hypothyroidism; chronic renal failure; diet high in cholesterol and total and saturated fat;
Pregnancy; cholesteryl ester storage disease; drug use (e.g. anabolic, steroids, beta – blockers, progestins, carbamazepine).
Decreased in
Severe illness; abetalipoproteinemia; some laboratories also various ratios; total cholestero/HDL ratio – low risk: 3.3 – 4.4, average risk: 4.4 – 7.1, moderate risk: 7.1 – 11.0, high risk > 11.0.High Density Lipoprotein (HDL) Cholesterol (Lipid Profile)
1. High Density Lipoprotein (HDL) Cholesterol
Introduction
Levels of HDL are inversely related to risk of CAD. For every mg/dL decreased in HDL, risk of CAD increase by 2 -3%
Indications
Assessment of risk of CAD
Diagnosis of various lipoproteinemia
Normal Levels | |
Men | Women |
> 40mg/dL | > 50mg/dL |
Increased in (60mg/Dl is negative risk factor for CAD)
Vigorous exercise; moderate consumption of alcohol; Increased clearance of triglyceride (VLDL), Familial lipid disorders with protection against atherosclerosis (illustrates importance of measuring HDL to evaluate hypercholesterolemia); 1 in 20 adults with mild increased total cholesterol levels (240 – 300mg/dL) secondary to increased HDL ( > 70mg/dL); Hypobetalipoproteinemia.
Decreased in (< 32mg/dL in men, < 38mg/dL in women)
Stress and recent illness (e.g. acute myocardial infarction [AMI], stroke, surgery, trauma); starvation, non fasting sample; obesity and lack of exercise; cigarette smoking; DM, hypo – and hyper – thyroidism; acute and chronic liver disease; genetic disorders; familial hypoalphalipoproteinemia.Total Serum Cholesterol (Lipid Profile)
ToTotal Serum Cholesterol
Indications
Monitoring for increased risk factor for coronary artery disease(CAD); Screening for primary and secondary hyperlipidemias; Monitoring of treatment for hyperlipidemias.
Normal range | |
Adults: 130 –20mg/dL | Fetal: 32 – 76mg/dL |
Increased in
Hyperlipoproteinemias; cholesteryl ester storage disease; biliary obstruction (stone, carcinoma, cirrhosis); von Gierke's disease; hypothyroidism; nephrosis (due to chronic nephritis, amyloidosis, renal vein thrombosis, systemic lupus erythematosus [ SLE]; Pancreatic disease, diabetes mellitus.
Decreased in
Severe liver cell damage (due to chemicals, drugs, hepatitis); hyperthyroidism; malnutrition; infection and inflammation; drugs.
Oral Glucose Tolerance Test (OGTT)
Oral Glucose Tolerance Test (OGTT)
Introduction
OGTT is done after overnight fasting for 10 –16 hrs. Certain drugs should be stopped several weeks before the test (e.g. oral diuretics, 0.Cs phenytoin). Loading dose of glucose [adults = 75gms, for children 1.75gm/kg (of ideal body weight in obese children but never > 75gms). Pregnancy = 100gms] is consumed in 5 mins. Blood sample drawn at fasting, 30, 60, 90, 120 mins.
Indications
OGTT should be reserved principally for patients with '' borderline'' fasting plasma glucose levels ( i.e. fasting range 110 – 140 mg/dL).
All pregnant women should be tested for gestational diabetes with a 50gms dose at 24 – 28 weeks of pregnancy; if result abnormal, OGTT should be performed after pregnancy.
Increased tolerance in
Pancreatic is let cell hyperplasia or tumor, poor absorption from gastrointestinal (Gl) tract in intestinal disease (e.g. steatorrhea, sprue, colic disease), hypothyroidism Addison's disease, liver disease, hypopituitarism.
Decreased tolerance in
Diabetes mellitus- For diagnosis of diabetes in nonpregnant adults, at least two values of OGTT should be increased (or fasting serum glucose > 140mg/dL on more than one occasion and other causes of transient glucose intolerance must be ruled out.
Other causes of decreased tolerance are hyperthyroidism, hyperlipidemia, steroid effect, Cushing's effect, administration of adrenocorticotropic hormone (ACTH) or steroids, pregnancy.
Drugs like indomethacin, various neuroactive drugs (phenothiazines, tricyclics, lithium, haloperidol), heparin.Blood Glucose
Blood Glucose
Indications
Diagnosis of diabetes mellitus [defined by World Health Organization (WHO) as unequivocal increase of fasting serum (or plasma) glucose > 126 mg/dl on more than one occasion or any glucose level > 200mg/dL]; Control of Diabetes Mellitus; Diagnosis of hyperglycemia.
Normal Range | |
Fasting | Post prandial (2hrs)
|
60 – 100mg/dL | < 140 mg/dL |
Higher levels seen in
Diabetes Mellitus including: hemochromatosis, Cushing's syndrome; acromegaly and gigantism, Increased circulating epinephrine due to – adrenaline injection, pheochromocytoma, stress, acute and chronic pancreatitis, effect of drugs like (corticosteroids, estrogens, alcohol, phenytoin, thiazides.)
Pancreatic disorders (e.g. Islet cell tumor, Pancreatitis, glucagons deficiency); extrapancreatic tumors (e.g. carcinoma of adrenal gland and stomach, fibrosarcoma); hepatic disease (e.g. hepatitis, poisoning, cirrhosis, primary or metastatic tumor); endocrine disorders (hypopituitarism, Addison's disease, hypothyroidism); functional disturbances (e.g. postgastrectomy, gastroenterostomy, autonomic nervous system disorders); pediatric anomalies (e.g. prematurity, infant of diabetic mother); enzyme disease (e.g. von Gierke's disease, galactosemia, fructose intolerance others like malnutrition, alcoholism, exogenous, insulin or oral hypoglycemics).Lower levels seen in
Activated Partial Thromboplastin Time(aPTT)
Activated Partial Thromboplastin Time(aPTT)
Introduction
aPTT is the best screening test for disorders of coagulation; it is abnormal in 90% of patients with coagulation disorders. Screens for all coagulation factors that contribute to thrombin except factor VII and XII. The test may not detect mild clotting defects which seldom cause significant bleeding.
Normal range
25 – 38 seconds
Indications and Interpretation
Monitor heparin therapy; Screen for hemophilia A and B,
Prolonged by
Defect in following factors: I, II, V, VIII, IX, X, XI, XII; Presence of specific inhibitors of clotting factors (most frequently antibody against factor VIII, in 15% of patients with hemophilia); heparin, warfarin and lupus anticoagulant.
Normal in
Thrombocytopenia, Platelet dysfunction, Von Willebrand's disease, isolated defects of factor VII.
Prothrombin Time(PT)
Prothrombin Time(PT)
Normal range
11 –16 seconds
Indication
Control of long – term oral anticoagulant therapy with coumarins and indanedione derivatives; evaluation of liver functions( PT is the most useful test of impaired liver synthesis of prothrombin complex factors[ factor II, VII, IX, Protein C & S]; evaluation of coagulation disorders- screen for abnormality of factors involved in extrinsic pathway (factor V, VII, IX, Prothrombin, fibrinogen). Should be used with a PTT.
Prolonged by defect in
Factor I, II, V, VII and X
Prolonged in
In adequate vitamin K in diet, premature infants, newborns of vitamin K deficient mothers, poor fat absorption (obstructive jaundice, colitis, steatorrhea), severe liver damage (hepatitis, poisoning), anticoagulant drugs, familial hypoprothrombinemia.
Coagulation Time/ Clotting Time (CT)
Coagulation Time/ Clotting Time (CT)
Normal range
6 –17 minutes (glass tube),
Indications and Interpretations
Former routine method for control of heparin therapy but now replaced by a partial thromboplastin time(PTT) as it is not a reliable screening test for bleeding conditions because it is not sensitive enough to detect mild conditions but only detects severe ones; normal coagulation time does not rule out a coagulation defect; routine preoperative bleeding and coagulation time are of little value for preoperative screening.
Prolonged in
Severe deficiency (< 6%) or any known plasma clotting factors except factor XII and factor VII, afibrinogenemia and presence of circulating anticoagulant (including heparin).
Normal in
Thrombocytopenia, deficiency of factor VII, von Willebrand's disease, and mild coagulation defects due to any causes.
Bleeding Time (BT)
Bleeding Time (BT)
Normal Range
3 – 9.5 minutes
Indications and Interpretations
· BT is functional test of primary hemostasis
· BT is single screening test for platelet functional or structural disorders, acquired (e.g. uremia) or congenital
· Normal BT without suggestive history usually excludes platelet dysfunction. However, a normal BT does not rule out significant defect; with clinical suspicion platelet aggregation should be performed
· To work up for coagulation disorders in patients, having history of excess bleeding even with normal platelet count.
· Normal in all other disorders of coagulation except von Willebrand's disease deficiency and some cases of very low plasma fibrinogen.
· May be useful to monitor treatment of active hemorrhage in patients with prolonged BT due to uremia, Von Willebrand's disease, congenital platelet function abnormalities or severe anemia.
· No value in performing BT if platelet count < 100,000/cumm as BT is usually prolonged. Prolonged BT with platelet count > 100, 000/cumm usually indicates impaired platelet function (e.g. due to aspirin) or von Willebrand's disease.
· Even with a prolonged BT, blood loss does not exceed that of patients with normal BT. Prolonged BT does not necessarily cause increased bleeding.
· BT increased out of proportion to platelet count suggests von Willebrand's disease or qualitative platelet defect.
Usually prolonged in
Thrombocytopenia: Platelet count < 100,00/cumm and usually < 80,000/cumm before BT becomes abnormal and < 40,000/cumm before abnormality becomes pronounced.
Platelet function disorders
Hereditary: Von Willebrand's disease, deficient release of platelet glycoproteins, gray platelet syndrome, hereditary hemorrhagic telangiectasia
Acquired: Drugs (aspirin, non- steroidal anti-inflammatory drugs [ NSAIDs], antimicrobials, anticoagulants, anesthetic, calcium channel blockers, β – blockers, phenothiazine, antidepressants), uremia, fibrin degradation products (e.g. disseminated intravascular coagulation [DIC], liver disease, fibrinolytic therapy, immune thrombocytopenias, myeloproliferative disease, vascular disorders, amyloidosis, viral infections, scurvy.
Usually normal in
Hemophilia, severe hereditary hypoprothrombinemia or hypofibrinogenemia.
Erythrocyte Sedimentation Rate (ESR)
Erythrocyte Sedimentation Rate (ESR)
Introduction
ESR is the rate at which RBC's settle down when blood, to which anticoagulant is added, is allowed to stand in a narrow tube for one hour expressed in millimeters of clear plasma at the end of 1st hour. Sedimentation rate depends on various factors like; rouleaux formation (Rouleaux formation is directly proportional to concentration of fibrinogen and globulin in plasma. It is retarded by albumin); viscosity of plasma (ESR decreases if viscosity increases); ratio of cells to plasma (decreased ratio leads to increase Rouleaux formation); nature of anticoagulant used.
Normal Range (mm in 1 hr) | |||||
Westergren | Wintrobe's | ||||
Males | Females | Males | Females | Children | Newborns |
0 –13 | 0 –20 | 0 –10 | 0 -15 | 0 – 13 | 0 -2 |
Increased in
Tissue damage or inflammation, anemia, any toxic or infective condition (acut or chronic), malignancies, nephrosis, physiological increase in females, pregnancy increase in temperature.
Decreased in
Polycythemia, leukemia, hypofibrinogenemia, pernicious anemia, congestive heart failure (CHF), Protein shock (e.g. burns, severe allergic reactions), physiological decrease in newborns, decrease in temperature.Reticulocyte Count (RC)
Reticulocyte Count (RC)
Introduction
The reticulocyte count is a fairly accurate reflection of erythropoietic activity therefore their number increases whenever red blood cells (RBCs) are being rapidly manufactured.
Normal Range
Adults: 0.5 – 1.85 % of erythrocytes, absolute count – 29,000 – 87, 000/cu.mm.
Newborn: 2.5 – 6.5 %, falls to adult range by second week of life.
Indications
· Diagnosis of inffective erythropoiesis or decreased RBC formation
· Increase indicates effective RBC production used as: Index of therapeutic response to iron, folate or vitamin B12 therapy and blood loss; monitor treatment response after bone marrow suppression and transplantation; monitor response to erythropoietin therapy.
Increased in
After blood loss or increased RBC destruction, after iron therapy, after specific therapy for megaloblastic anemia and other hematologic conditions like polycythemia, metastatic carcinoma in bone marrow.
Decreased in
Ineffective erythropoiesis or decreased RBC formation (severe autoimmune type of hemolytic disease, megaloblastic disorders), alcoholism, myxedema.
Wednesday, August 11, 2010
Abnormally shaped RBCs Spiculated
Abnormally shaped RBCs Elongated
Abnormally shaped RBCs Round
Abnormally shaped RBCs
Round – Macrocytes (increased erythropoiesis); round macrocytes (liver disease, hypothyroidism, alcoholism); macro – ovalocytes (megaloblastic anemia, cancer chemotherapy, myelodysplastic syndromes); microcytes (hypochromic anemias), spherocytes (hereditary spherocytosis, recent blood transfusion); stomatocytes (hereditary stomatocytosis, acute alcoholism); target cells (HBC disease or trait, HbD, HbE, HbS, thalassemia, iron deficiency anemia, liver disease, post splenectomy).Peripheral Blood Smear (PS)
Peripheral Blood Smear(PS) - RBCs
Indications
Peripheral smear is done for typing anemia, to confirm red blood cells (RBC) indices or indicate leukemia or other conditions,
RBC inclusions
Basophilic or polychromatophilic macrocytes ( < 15 in healthy persons, increased in erythropoiesis due to hemorrhage or hemolysis); microcytes with stippling (thalassemia, lead poisoning); Cabot's rings (severe hemolytic anemias, pernicious anemia [ PA]); Howell – Jolly bodies(megaloblastic anemia, thalassemia, hyposplenism, splenectomy); Pappenheimer bodies (Sideroblastic anemia, thalassemia, lead poisoning, pyridoxine unresponsive or responsive anemias); Heinz bodies (congenital G – 6 PD deficiency, drug induced hemolytic anemias); Plasmodium trophozoites(malaria); reticulocyte.
Thrombocytopenia (Decreased Platelet Count )
Thrombocytopenia in
Bone marrow depression, hypersplenism, viral infections (especially in dengue fever), drug hypersensitivity, antiplatelet antibodies (lgG and lgM), increased platelet consumption in thrombotic thrombocytopenia (TTP), disseminated intravascular coagulation (DIC) and septicemia.
Thrombocytosis (Increased Platelet Count )
Thrombocytosis in
After administration of epinephrine due to splenic contraction or after splenectomy, trauma (e.g. surgery, injury, childbirth) and stress.
Causes of eosinophilia (> 250/cu.mm. diurnal variation with highest levels in morning)
Causes of eosinophilia (> 250/cu.mm. diurnal variation with highest levels in morning)
Allergic diseases (bronchial asthma, hay fever, urticaria, allergic rhinitis);
Parasitic infestations, mycoses, scarlet lever, erythema multiforme systemic lupus erythematous, rheumatoid arthritis, skin diseases (e.g.pemphigus).Causes of monocytosis ( > 10% of differential absolute count > 500/cu.mm.)
Causes of monocytosis ( > 10% of differential absolute count > 500/cu.mm.)
Monocytic leukemia, other myeloproliferative disorders, lymphomas, lipid storage diseases, post splenectomy, protozoal and some rickettsial infections, SBE, tuberculosis, brucellosis sarcoidosis, rheumatoid arthritis, systemic lupus erythematosus(SLE).Causes of basopenia
Causes of basopenia
Hyperthyroidism, pregnancy, irradiation, chemotherapy, glucocorticoid administration, acute phase of infection.
Basophilia (50/cumm or > 1%)
Basophilia (50/cumm or > 1%)
May be first sign of blast crisis or accelerated phase of chronic myelocytic leukemia (CML).
Persistent basophilia may indicate unsuspected myeloproliferative disease.
Causes
Chronic myelogenous leukemia, basophilic leukemia, polycythemia, myeloid metaplasia, Hodgkin's disease, chronic sinusitis and hemolytic anemia.
Causes of lymphocytopenia (Decreased Lymphocytes) (< 1500 in adults, < 3000 in children)
Causes of lymphocytopenia (< 1500 in adults, < 3000 in children)
Increased destruction (chemotherapy or radiation treatment, corticosteroids),Causes of lymphocytosis (Increased Lymphocytes) (> 4000/cumm in adults, > 7200/cumm adolescents, > 9000/cumm in children and infants)
Causes of lymphocytosis (> 4000/cumm in adults, > 7200/cumm adolescents, > 9000/cumm in children and infants)
Infection (Pertusis, infectious, lymphocytosis, infectious hepatitis, cytomegalovirus (CMV) infections, mumps, rubella, varicella, toxoplasmosis, chronic tuberculosis),
Others like
thyrotoxicosis,
Addison's disease,
neutropenia with relative lymphocytosis,
lymphatic leukemia,
Crohn's disease,
ulcerative colitis and
infancy (normal count 40- 60 %) called relative lymphocytosis.
Causes of Neutropenia (Decreased Neutrophil) (Absolute count < 8000/ cu.mm.)
Causes of Neutropenia (Absolute count < 8000/ cu.mm.)
· Infections: bacterial (e.g. overwhelming infection, septicemia, typhoid, paratyphoid) viral infections (infectious mononucleosis, hepatitis, influenza, measles, rubella), rickettsia, others (malaria, kala- azar).
· Infants (normal count 40%).
· Hodgkin's disease, chronic sinusitis, hemolytic anemia and lonizing radiation
· Drugs & chemical (antibiotics, analgesics, antithyroids, arsenicals and ionizing radiation
· Hematopoietic diseases (aleukemic leukemia, aplastic anemia) and splenic sequestration.
· Autoimmune and isoimmune neotropenias.
· Immune defects like infertile genetic agranulocytosis.
Causes of Neutrophilia (Increased Neutrophil) (Absolute count > 8000/ cu.mm.)
Causes of Neutrophilia (Absolute count > 8000/ cu.mm.)
· Acute infections:
· Localized (e.g. Pneumonia, meningitis, tonsillitis).
· Generalized (e.g. acute rheumatic fever, septicemia, cholera).
· Inflammation (e.g. vasculitis).
· Intoxications: metabolic (e.g. acidosis, uremia, acute gout); Poisonings (e.g. mercury, epinephrine, black widow spider bite).
· Acute hemorrhage or hemolysis of red blood cells.
· Tissue necrosis (e.g. acute myocardial infarction [AMI], burns, gangrene).
· Physiological (e.g. exercise, Stress, obstetric labor, menstrution).
Tuesday, August 10, 2010
Differential leukocyte Count (DLC)
Normal Range | |||
Granulocytes | Percentage | Agranulocytes | Percentage |
Neutrophils | 54-62 % | Lymphocytes | 20- 40 % |
Eosinophils | 1-4 % | Monocytes | 3-7 % |
Basophils | < 1 % |
diagnosis of myeloproliferative disorders;
neutrophil and band counts may be useful in acute appendicitis and
neonatal sepsis with moderate sensitivity and specificity